Natural Systems Theory

by Hugh M. Lewis

http://www.lewismicropublishing.com/

 

   Chapter Thirteen

The Cell as a Living System

 

            The biological sciences are considered the most paradigmatically unified fields of modern science. It is not just the theory of evolution which helped to provide unification to otherwise disparate fields of biological study. In fact, unity of the subject is implied by the Grand Unity of Living Systems on earth, the fact that life probably arose once on earth, and has been continuous in its divergent evolution of new life forms, and hence all living systems are part of a common tree of ancestry reflected by shared genetic structures and common molecular configurations.

            Less well known than Darwin's theory of Natural Selection,Cell Theory emerged about twenty years previously, as a product of a couple centuries of close observation and recording of life forms at a microscopic level. This theory, called the Cell Doctrine, was first published in 1838-9 by T. Schleiden and M. Schwann, stressing that cells are the universal component of living organisms, and subsequently developed to a modern synthesis by the Twentieth Century, as more was learned about the cell's structure and behavior.. In short form, it first threee tenets holds three fundamental principles of living systems:

 

            1. Every organism is composed of one or more cells.

            2. The cell is the smallest unit of organization having the properties of life (i.e., growth and reproduction)

            3. The continuity of living forms arises as as consequence of the growth and division of single cells.

 

John Baker provided a more thorough historical synopsis of Cell Theory:

 

1. Most organisms are composed of a large number of microscopic cells.

            2. All cells share similar defining structural characteristics.

            3. Cells always arise from preexisting cells through reproduction.

            4. Cells constitute the living tissue of organisms in which new material is synthesized. Non-cellular material is extruded by cells or built of transformed cells.

5. Cells have an individual character somewhat independent of the organism as a whole

6. Cells of multi-cellular organisms correspond in certain respects to the body of a protist or single-celled organism.

7. Muli-cellular organisms probably arose from the colonization of protists.

 

A modern synthesis of Cell theory is given by the following tenets:

 

            1. All cells store information in DNA

            2. Genetic information is the same in all species of cells.

            3. All cells decode genetic information using RNA transcription and translation.

            4. All cells synthesize proteins by means of ribosomal RNA translation

            5. Folded protein structures (enzymes) govern the activities, functions and morphological structure of all cells.

            6. All cells utilize ATP as the main medium for energy utilization.

            7. All cells are enclosed by a plasma lipid-protein membrane that serves as a boundary layer through which there is an exchange of molecules.

 

Cells are in many ways the prototypical general system, albeit on a microscopic scale. It was indeed the problem of the Cell, then a relative Black Box, that drove Ludwig von Bertalanffy, a biologist, to develop General System Theory. Cells have many of the prototypical characteristics of a general system model: a boundary layer, feedback mechanisms in the form of enzymes that facilitate or inhibit biochemical reactions, and selective transport mechanisms that mediate between the inner environment of the cell and its external environment. The size of cells are critically related to their capacity to efficiently transport nutrients and other chemical agents through the cell and from outside into the cell.

Cells perform to basic dynamic functions that are also archetypically general system based--their main functions are 1) the utilization and acquisition of energy for self-maintenance and growth, and the 2) replication, transcription, translation and reproduction of critical information (DNA). These fulfill two of the basic paradigms of dynamic systems--information and energy transaction.

The cell is the fundamental construct of living systems. It is the common building block of all living tissue and the foundation for all living systems, without exception. In many ways it is the best example of a prototypical system that we can conjure up, and it is in many ways the epitome of natural self-organization. Indeed, general systems science really had its birth in the concern with holistic perspectives upon cellular function and development, at a time when the internal organization and happenings of a cell were still pretty much a mysterious "black box." We need only consider how remarkable cellular evolutionary development has been, when we realize that all living organisms have been basically the descendants of a continuous, non-stop process of cellular growth, reproduction and division from the first proto-biotic cellular formations, and it is possible that all life might have originated from a single successful cellular system. I return to the examination of the cell as a system, for beyond ecology, what little formal biological study I've had has been focused upon the cell.

A systems based perspective upon the cell therefore would be based upon not only the examination of the metabolism, behavior and life-cycle of a cell as a prototypical biological system, but upon what can be called "cell ecology" and properly "cellular meta-biotics" or the nature of inter-cellular interactions that influence the outcomes of microbial development and evolution. At some point, microbial populations would begin exerting a significant influence upon their environment, and begin altering their bio-geophysical contexts in the direction that encouraged further evolutionary development taking place. In spite of the self-containing environment within the cell membrane, all cells exhibit specialized environmental adaptations. They exist in rather special and narrow contexts of cell development, that define the limits of their growth and development.

Under normal conditions for a cell, a cell can be expected to respond to its environment by growing in population to the natural limits of its context, and then overstepping these limits in critical ways. Death rates will eventually balance or exceed reproductive rates, and the population will eventually crash or achieve some long term equilibrium.

A phenomenon called "endosymbiosis," the encapsulization of the DNA machinery of one micro-organism by another, and the appropriation of that machinery, seems to me a fitting demonstration of a systems-based meta-biotic framework. Virus's and viroids are similar entities, that, though associated with disease, demonstrate a kind of meta-biotic complication of living systems that do not fit normal hierarchical frameworks. Horizontal transmission of DNA, especially in some forms of soil bacteria, are another case that clearly defies our received models of strict vertical and intergenerational transmission of DNA from parent to offspring.

"Endosymbiosis" becomes the basis for the emergence of Eukarya, more complex cells, and in turn for multi-cellular organization, which features functional subordination and specialization of cell types. A fertilized gamete will carry the blueprints that include the instructions for the development of a large number of different specialized cell types performing a host of integrated functions. The differentiation of so many cell types from a single precursor resembles the controlled internalized embodiment of the entire process of taxon evolution of complex forms from simple parent cells. 

It is evident therefore in the first place that all cells are capable of evolutionary development and speciation through chance genetic variation of structure. Microorganisms have been observed to be capable of quite rapid speciation and evolutionary development, compared to more complex living systems that are slower to replicate and reproduce. The earliest known form of cells, presumably some primitive form of Prokarya, were of minimal possible size and structure, probably less than five micrometers in diameter and a micron in thickness. This was perhaps the optimal size for rapid self-replication and immediate exploitation of whatever growth medium becomes available. It seems that life seized on the basic principles involved in this, and capitalized on it as much as possible.

It is the case therefore that in the war against disease, there is a on-going struggle to develop effective vaccines against new strains of old strains of bacteria that become immune to previous remedies through evolutionary adaptation.

The principle function of the cell can be said to provide a suitable environment for the storage and replication of DNA and the machinery needed for this storage and replication, as well as for replication needed for the components of the cell itself. A cell must therefore be capable of faithfully reproducing its DNA informational database, and itself. It requires transportable and usable energy, in chemical form, for carrying out its many tasks, and it must be capable of somehow capturing and transporting energy into itself across its membrane. Cellular reproduction is a normal part of cell growth and its life-cycle. 

Essential components of cells, besides DNA, are:

 

1. A cell wall and/or cytoplasmic membrane

2. Cytoplasm

3. A nucleus or nucleoid

4. Cellular Organelles, consisting of ribosomes and/or mitochondrioon, endoplasmic reticula for the manufacture of proteins and for the maintenance of cellular tissue structure, function and equilibrium.

 

The first distinction we draw is between simple bacteria or prokaryotes, and complex cells referred to as eukarya or eukaryotes. In general, prokaryotes are much smaller and simpler than eukaryotes, averaging between 1 and 5 micrometers (versus about 25 micrometers for eukarya) and about 1 micrometer in depth. They have a cell wall, but otherwise lack many of the structures common to eukarya. 

Prokarya are simple one-celled organisms capable of fairly rapid reproduction. They are presumably the first organisms, or the direct descendants of the first forms of life, to have evolved on earth. Some have even suggested the possibility that they may have been carried to earth in a meteorite that crashed in the best of circumstances (cosmic seeding hypothesis), and from there began reproducing and evolving. Prokarya are grouped into bacteria and archaea, distinguished largely by the complex structures of the cell walls and analytically by their growth characteristics in various mediums and the ability to stain under a cover slip of a microscopic slide. 

Eukarya evolved from Prokarya, with the suggested mechanism of the symbiotic ingestion ("endosymbiosis") of one cell by another to form a more complex structure of organelles like mitochondria and chloroplasts. Eukarya include algae, fungi, protozoa and all multi-cellular life forms we know of. Prokarya in general do not form multi-cellular structures of any form. They lead an independent life contained within the narrow confines of their cell wall. Under the right conditions, they are known to grow rapidly, which growth is defined by the cellular division and propagation by mitosis at a fairly fast doubling rate.

One possible scenario of the development of proto-life was that the first forms to emerge were primitive extremophiles, Archaea, that developed through chemosynthesis. These eventually differentiated and evolved into forms that were less marginal and more tolerable of normal conditions, and that possibly could find a broader range of energy resources. From these developed what we know of as the prototypical generalized bacteria. This bacteria became so successful as an environmental generalist, that the first adaptive radiation of life was its spread by air, water or any other medium to virtually the entire earth, to cover the whole earth in a thin, invisible layer of life. When this prototypical bacteria encountered extreme conditions, it possibly resumed characteristics of an extremophile form.

One of the main functions of the cell-membrane is to provide a medium for transport between the external environment of the cell and the cell's self-maintaining internal environment. We know from the standard general system model that such transport mechanisms and mediums are fundamental to the definition of systems as order creating and order maintaining processes. The cell membrane, therefore, with or without the added structural or buffer support of a cell wall, is a vital component of all cell systems, for they are the principal transport mechanisms of such systems that maintain internal equilibrium and stability of the internal environment across a random and external environment.

In the case of multi-cellular organisms, we must ask what a cell gives up in terms of its independence as a system, and what it gains in turn from the specialization of function and structures. Specialized cells tend to take on definite shapes and configurations of structure, and they tend to be capable of performing fairly specialized functions, either in a chemo-mechanical manner or in terms of the production of special protein structures or cellular metabolism. What is clear is that such cells, in become specialized, become dependent upon the organismic contexts in which they develop--they cannot survive apart from the super-cellular structures in which they develop.

It is clear that from fairly early on cellular evolution became a meta-biotic process, with cells respond to and adapting to the presence and behavior of other cells as a part of their environment. The most basic form of this kind of interaction was probably competition of different strains of bacteria for the same resource substrates. Selection that we can observe at this level is generally geared to those strains that can effectively tolerate, adapt to and exploit a different medium. Symbiotic or complementary relationships between different strains of bacteria may have developed in time. 

The earliest mechanisms of cellular metabolism (catabolism and anabolism) was presumably some form of chemo-synthesis--the derivation of usable chemical energy from some form of enzyme reaction with a chemical substrate. Presumably, one of the first metabiotic forms of relationship that may have developed between different species of bacteria may have been that of predator-prey relations, or the capacity for one strain of bacteria to attack and consume another form of bacteria for its energy and material reserves. Photo-synthesis was known to have evolved from early Eukarya, and presumably one of the first forms of endosymbiosis may have been in terms of photosynthetic cloroplasts capable of synthesizing chemical energy from the energy of the sun. Indirect symbiosis and interdependence also undoubtedly occurred, by which the action and metabolism of one organism created the environment suitable for the growth of a second organism.

Presumably, though there are many kinds of Prokarya we know of today, their basic structure and function is not so very different than that of their original precursors, and the diversity of life forms at this level appears to be far lower overall than the diversity of more complex multi-cellular organisms. Of all varieties of prokarya, the forms possibly most similar to the ancestral "precursor" of life are possibly the archaea though what we know of these prokarya today is that they have fairly specialized cellular membranes and walls.

 

The Cell as a Self-Replicating System

 

There has been an unusual unity of living systems. From the organization of the first successful prototypical cell, there has been a line of continuous self-replication and pattern variation that has led through the entire natural history of evolution. In other words there has been an unbroken chain of cells that have successfully reproduced themselves. Life seems to have evolved only once, and once having achieved successful reproduction or self-replication, its lines grew and diversified and never, as a whole, died out over billions of years.

All living organisms are cellular, and we can study all life as we know it on earth from the standpoint of the cell, its reproduction and adaptation and its normal life-cycle.

The primary function of all cells is that of self-replication, therefore the minimal amount of machinery-information necessary to successfully achieve such self-replication is the primary requirement of cell growth and metabolism.

The first cells had to have had at least a cell wall, cytoplasm, ribosomes plus RNA transcription/translation structures, and some kind of DNA bound to a nucleoid structure.

The functions of DNA are:

 

1. Its own copying.

2. Creation of structures that allow its copying.

3. Creation of the cellular structures that permit the cell to survive as a distinct system.

4. Adaptation to varying environmental conditions.

 

In other words, the original and all subsequent DNA had first 1) to replicate itself; 2) to replicate the replication machinery; 3)to replicate the cell as a house and factory for replication; 4. Perform necessary cellular metabolism which involves energy-matter transactions with its environment.

Cells perform secondary functions relating to their adaptation in varying environmental circumstances.

 

DNA as a Sequencing Clock regulating Cyclical Cell Growth

 

Cell growth and reproduction consists of a regular cycle that occurs with fairly precise timing and periodicity. This suggests that growth and self-replication is well regulated by a clock that is related to the length and complexity of the central DNA and the related RNA transcription/translation subcomponents that are necessary to complete the cycle. It is also known that environmental factors, such as ambient heat, light, relative presence or absence of nutrients or inhibitors, can slow or accelerate this cycle substantially, and that there must be some maximum rate at which such reproductive cycles can occur under the most optimum and ideal of circumstances, which appear, for most organisms, to be rarely obtained in natural environments.

I suspect that the cyclical process of DNA transcription/translation underlying cellular growth and reproduction involves a cascading time-table of complex reactions and interactions of cellular subcomponents, the complexity of which increases exponentially with time along a logarithmic curve.

It is also known that cellular metabolism and subcomponent reactions/interactions may occur at relatively high rates of speed, especially when mediated by enzymes.

Cell replication and cell growth/metabolism follows a clock, and this clock is the period required for a cell's complement of DNA to perform its series of functions, on a scheduled time-table, until the cell divides through cytokinesis and becomes essentially two new cells.

In a sense, bacterial or cancer cells do not die from old age--an older cell  becomes two newer cells. Only in eukaryotic multi-cellular organisms, where cells have specialized secondary functions to which cell growth is subordinate, can we speak of a cell death that occurs as the product of the expiration of the organism.

A multi-cellular organism is a highly organized community of cells, so well organized that the community has organismic properties and functions that transcend the functions of individual cells or cell tissues.

DNA as a clock is the amount of time required for the DNA to undergo complete transcription and for all subsequent translation subprocesses to be continued. It is likely that these processes involve to some unknown extent reiteration of transcription and translation, and this reiteration or recursion itself must be controlled somewhat dynamically by the DNA, or else this control comes built into the structure of the DNA sequencing (and "con-sequencing") itself.

If we look at simple bacterial reproduction, cytokinesis is followed by a latency period during which the cell itself must increase in size to reach the normal limits of a prokaryote. This form of morphological growth or expansion of the body of the cell must involve the cell being busy with the process of manufacturing its own equipment and organic resources from the natural substrates of its environment, up to its own internalized limits or carrying capacities. At this stage, the process begins repeating itself as a cycle.

 

The Cell and DNA Transmission Mission as a Natural Computational Device

 

The amount of information contained in the DNA strand of even a simple bacterium is indeed staggering, much less the full diploidal complement of information, for instance, found in any given cell of the human body, with its normal complement of 46 chromosomes reproducing the entire library of the human genome. When we furthermore consider the millions of cells that make up the various tissue structures of our body, with but few exceptions of specialized cells like red corpuscles, etc., we end up with a staggering set of statistics--a tremendous amount of information stored in spaces so small that they cannot even be seen under the normal maximum magnification of a light microscope. These kinds of considerations substantially diminish the significance of  our own recent achievements in informational manipulation and storage, of which we are so amazed.

DNA codon structure is founded upon the pairing of four nucleic bases, in two complementary pairs each. This structure is necessarily quaternary, versus the binary structures of our own digital-electronic systems. A three codon series or unit yields a total of 64 possible combinations (4 x 4 x 4) which it would require a six codon series of a binary system to yield as many combinations (2 x 2 x 2 x 2 x 2 x 2). This strikes one as a inherently much more efficient, faster and versatile system than achievable with binary encoding alone. In a vulgar sense, chromosomes with binary encoding would have to be twice as long and large and would problem require twice the amount of time for transmission to occur overall. That as we know it now only 21 of the total number of 64 combinations are needed for making all known protein structures, allowing for redundancy and substitution of alternate codons for the same structures, allows not only an increased flexibity but also an increased stability in the system.

In a sense the primary function of the cell, in being self-replication, serves as a computational device the primary purpose of which is the reading, transcription and translation of the DNA code it contains. This DNA code is therefore somewhat analogous to the software that drives the functioning of a computer to create a meaningful informational output. This kind of computational device quickly reaches the scale of a microscopic, parallel processing supercomputer--the simple act of reading the DNA code along a strand quickly becomes the multiple events of RNA sequences  being translated into a very wide range of proteins serving multiple functions.

If we wish to push this analogy with artificial intelligence, then we must imagine a computing device that is capable of recreating and reproducing its own hardware, of building from its available, self-made store-house and factory of components two new computers.

 

Living systems have had four billion years to develop its range and depth of forms and structures that we understand it today. It is likely that for much of the first billion years replication was fairly confined to a few limited and relatively simple life-forms. These early systems had to solve basic problems through systematic variation of pattern--something like a super-computer that must run at high speed day and night for a considerable length of time, to achieve a new solution to complex problems.

The evolutionary exploration of new solutions to problems of self-reproduction and adaptation by living systems is regarded in a strict sense as "blind" being ultimately based upon a randomizing agency of encoding error or genetic mutation, but the search achieved through diversification and exponential increase in living systems was nonetheless systematic and deterministic in that it resulted in the long run in stream-lined optimal solutions to complex problem sets. This systematicity was largely achieved by a kind of blind but compulsive "trial and error" in which successful learning could only be measured by successful adaptation of emergent forms and properties of living systems and by what can be called, in the structure of the long run, taxon progress.

Looking back, among a long trail of discarded evolutionary experiments and legions of dead hulks and extinct sympatric species, we find a series of mile-stones of evolutionary achievements that opened the doors to the emergence of entire new lines and taxons of organism.

To the extent that we consider DNA as a natural informational encoding device, and its transmission and translation into alternate protein structures and functions, as a dynamic (i.e., non static) form of informational processing, we must take the informational model of living systems somewhat seriously and we must not dismiss the idea that from the beginning the primary function of living systems, of all life in general as we know it, has been one of computational self-replication.

Things like human intelligence, our big brain, and mammalian intelligence in general, however instinct driven and determined, must by comparison be seen primarily as the spin-off properties of emergent complexity, secondary derivative functions of living systems that have been serving first and foremost, without exception, its primordial, original function of cellular self-replicaiton.

 

Microscopic Life Forms

 

The DNA transcription process is the universal code of life, and these result in the production of a very large array of complex proteinstructures occurring within cellular matrices that can be said to be the universal building blocks of all life. If we want to understand the basic structure of all living things, then we must understand the structural patterns of life upon these basic microscope levels. These basic molecular structures are found in all living forms, and their dynamics constitute the foundation for understand the patterning and behavior of all organic systems. It is likely that living systems outside of our terrestrial system may assume completely new shapes and forms based upon their essential amino acids that will be different than our own, and result in entirely different protein structures. Of course, many of the structual and basic mechanics of the two systems will be virtually the same or convergently similar.

            It is difficult to think of a large Sequoia tree as a huge multi-cellular system that perpetuates itself through time and periodically regenerates and replicates itself as other individual organisms. These cells are differentiated in form and function based upon their specialization within the larger cell matrix of the giant tree, and these form various functions in coordination with one another to maintain the tree as a living organism. Similarly, when we think of a whale that sounds the depths of the ocean, we do not normally think of it as a vast complex of cells growing together in unison to compose a single organism. The behaviors we attribute to the whale, its whistles and clicks, its diving and breaching, its migration from north to south and back again, its social behavior and nurturance of its offspring. They are difficult to explain only in terms of the cellular components that make up the tissues of the whale. These behavioral traits that we may attribute to whales as inherent instinct are difficult to explain in terms of the analysis of the cellular systems that compose the whale and underlie its behavior.

 

Cellular Ecology and Evolution

 

Cellular, or microscopic ecology is a study of the processes of biological systems and their organization at a microscopic level. We cannot really understand macro-ecological systems until we can explain micro-ecology. The first cellular organisms arose in certain environments that was conducive to their survival and propagation. These conditions have been maintained, or even influenced, by life forms, and to a great extent life forms have evolved upon a cellular level in such a manner as to incorporate a protected cellular environment into a larger multi-cellular system. The result of this process is the ability for life forms to create their own internal environments, and internal ecologies, that are necessary for the survival of their cellular populations. At the same time, specialized functions must be developed, in terms of motility, response, recognition, etc., that allows these cellular organizations to effectively mediate with an external environment, and to achieve thereby a dynamic equilibrium between the external and internal world. The evolution of multi-cellular systems was largely the function of this kind of dynamic equilibrium established early on and perpetuated and elaborated into many different forms of life that we witness today.

            If we confine ourselves strictly to the microbiological level of analysis of ecological and evolutionary processes, introducing larger level considerations only as control mechanisms in such systems, then it is possible to develop basic models of such processes that can be said to be true of a broad range of life in general. In general, we may say that all cellular life-forms require certain stable external conditions for their survival, metabolism, growth and reproduction. All cellular life forms will reproduce at basic rates, and the variation of these rates of reproduction for cellular forms are more or less equal. These rates, and metabolism and growth, will be influenced by the ambient temperature and the fluctuations and overall stability of this temperature through time. We may properly speak of micro-climates within which cell-growth and reproductive functioning is optimized.

            From the standpoint of energy dynamics and rate laws affecting biochemical reactions and properties within cells and between cells, we can see all cells as representing heterogenous second-order systems that mediate boundary phase-transitions of basic molecules--internalized surface areas that are the product of reticulation and convolution of cellular membranes and structures is critical to the control of the rates of these reactions. The phase transitions possible within the context of a cell are gas to solid, liquid to gas, and liquid to solid type reactions. The common components of these reactions are the basic elements and compounds found in cell structures and molecules, and water. Most phase transitions therefore can be said to be mediated within the framework of water as both a solvent for solutions and as a substrate for the transport of more insoluble molecules. These reactions tend to be complex, relatively fast and recurrent, and continuous through the life of the cell. The cell does not normally appear to shut down for a long period of dormancy or inactivity.

            Most cells as they have evolved, depend upon the critical presence of other kinds of cells for their survival. Most cells can be said to be metabiotically interdependent. Only some of the most basic forms of life, prokaryotic bacteria, can be said to exist in a form that is relatively independent of the presence of other forms of life.

 

1. These forms have evolved basic means of independent locomotion to enable them to carry themselves to environments that are suitable for their functioning and survival, or else they rely upon physical forces for their transport.

2. In the absence or loss of suitable growing conditions, these kinds of organisms may otherwise become dormant and form spores that allow them to survive for very long periods of time until conditions arise that trigger their release and allow their growth to continue. This period of reactivation can be fairly rapid.

3. These organisms have a well defined cell-wall that serves to protect them their external environment and to mediate relationships with their environment.

4. Though many of these organisms may be parasitic or symbiotic with other forms of life, many of them are capable of extended growth under fairly abiotic conditions as long as these conditions provide the necessary physical factors for this growth to occur.

 

All other derivative forms of life have evolved in such a manner as to be dependent in one way or another upon other forms of life for their growth and survival, either in a directly mutualistic manner, or else indirectly through participation in a metabiotic system that fosters a shared bio-geophysical context suitable to life. Under such metabiotic conditions, we would expect that all forms of life would exhibit the following bio-physical characteristics:

 

1. The ability to be transported to favorable locations or away from unfavorable locations, either actively or passively by means of physical transport mechanisms.

2. The ability to either maintain internalized conditions in metabiotic contexts that achieve a degree of dynamic equilibrium with the environment in terms of heat and nutrients, inspite of external fluctuations of these conditions, or else a derivative capacity to limit functioning during periods that are beyond the optimal range of functioning.

 

If these biotically dependent organisms cannot achieve either of these functions independently, then they must be achieved in mutual relation with other organisms. They must achieve a degree of cooperative organization and functional interdependency that allows the cells to provide a common context for the survival of all the cells together.

            All unicellular organisms will reproduce at a set rate, and will automatically follow a principle of reproductive maximization under favorable conditions. Cellular forms of life will follow, under optimal conditions, standard rates of reproductive activity. Cell longevity will tend to be an average function of regular cellular regeneration and replacement.

            It appears that cellular systems, in metabiotic contexts in which their reproductive potential is constrained by requirements of metabiotic survival, will not be expected to undergo a process of reproductive maximization as would be expected of independent unicellular forms. Their relative specialization of function would result in the creation of external equilibrium conditions that would entail an sub-optimum reproductive rate. This is perhaps in part accounted for in terms of the basic differences between prokaryotic and eukaryotic organisms, and especially in terms of the nuclear DNA sequestration that occurs with the eukaryotic as opposed to that of the prokaryote.

In general, eukaryotic cells are larger and more internally differentiated that the prokaryotes. Within such an arrangement, cellular replication and division can be regulated by other mechanisms that occur within the cellular environment. Just as such cells are capable of regulating their rates of reproductive development within the metabiotic context of other cells, they are capable of yielding this reproductive capacity over completely and to only carry out simple cell division through mitosis without conjugation. Such cells, within a more complex biological program, are also capable of developmental differentiation through an extended life cycle of the larger organism, during which cells will divide and grow into different shapes, forms and functions. Such cells accomplish this process that represents a kind of encapsulated evolution--the capacity of the cell to divide into functionally different kinds of cells in the metabiotic context of the host organism.

            We may speculate on some of the following principles:

 

1. Cells requiring greater metabiotic functions of specialization generally tend to have more DNA to record and translate these structures.

2. Cells having longer and more DNA sequences will tend to divide or reproduce at slower rates, because transcription processes for long DNA sequences take longer to transcribe.

 

We may add one more kind of observation:

 

            On a microscopic scale of measurement, relatively small and discrete differences in intial states can lead to major differences in outcomes.

            Some DNA structures may be repeat, or "back-up code."

            Some DNA structures may be archaic survivors that are neutral.

            Some DNA structures may be "critical," others intermediate, and the remainder epigenetic in terms of their outcomes and effects.

 

            Thus, genetic modifications that affect repeated or archaic structures may have no consequences for the organism beyond possibly the increase in genetic load or the gradual erosion of any built-in evolutionary inertia in such systems.

            Furthermore, it is possible as well that some DNA may be active, or dominant, and other may be passive or recessive. Alterations that occur to active or dominant DNA structures may grossly affect the final outcomes, or else cause otherwise passive or recessive DNA to become more manifest and pronounced. It is possible that DNA may be variously switched on or off depending on the type of alteration to the coding sequence.

            It is evident from the observation of evolving traits of organisms that such evoltion tends to be trait specific, relatively continuous, and to exhibit a differential in terms of the relative plasticity to those that appear to be evolving rapidly, hypothetically as the result of differential selective pressures, and those other trait complexes that appear to be stable and non-evolutionary. Whatever conditions, for instance, that favored the development of larger and larger brains in the hominid line, these conditions must have been long-term and relatively stable over time, and it is apparent that it resulted in relatively greater plasticity of the hominid brain or related traits, for instance nerve structures and cranial and other related structures, such as the face, compared to other anatomical features such as the big toe or the ball of the foot.

            Therefore, though rates of genetic mutation or transcription error may be relatively low, comparatively minor alterations can result in major variations of pattern at higher levels. These outcomes would tend to be chaotic in their patterning.

            Upon the microscopic level, trait variation will be expressed in terms that tend to be trait specific to the form, type, size, shape, and function of the tissue structure that is involved.

            Upon a metascopic level of the organism, trait variation will tend to include both specific trait variations (eye color, hair follicle shape, etc.) as well as general variation of forms and features.

            The cell contains the entire DNA code for the entire mature organism. It is clear that any particular cell, at any stage of the growth and development of this organism, will use only a portion of this DNA code for its transcription, and this may be regulated in a number of ways--the presence of regulator DNA that switches some on and off in different schedules; the presence of a regulator DNA that encodes all the different developmental pathways that cells may take in the functional development of an organism; the relative presence or absence of similar or different cells in a sub-metabiotic context that provides the conditions for the signaling and further differentiation of cells. There would be some terminal path-end, at which point the cell would stop dividing and differentiating, and assume a function of simple growth and replacement.

            One must entertain the challenge of being able to write a single kind of equation that would, in its chaotic reiteration, result in the development of a differentiated organism in a predictable manner. There may be no single equation, but a set of interrelated equations, that accomplish such a function. In this manner, how is it possible that DNA might function in a manner that is programmable, and in a manner that may exhibit some form of fundamental organic intelligence in terms of the processing of complex information as a kind of biological algorithm or complex function.

            To some unknown extent, external prevailing conditions in the metabiotic environment may serve to regulate such patterns of growth and development as well. Intercellular commication or other forms of interaction may provide necessary components in the overall direction and control of such developmental differentiation.

            To the extent that there is inherent structural variability and flexibility in the encoding and transmission process, and to the extent that a cellular system can be said to be underdetermined, then the final outcomes of expression will be a function of phenotypic influence by the environment upon the system as a whole. Phenotypic flexibility can combine with genetic plasiticity of trait-complexes, to produce rapid rates or variable of evolutionary transformation of structure. Phenotypic flexibility and genetic plasticity can result in a kind of feedback system that favors differential trait selection. Phenotypic flexibility of the expression of a trait complex would result in differential selective pressures and adaptive functioning of different organisms.

            We see phenotypic flexibility in the ontogenetic development of many organisms--many derivative structures and patterns of organisms are unique to that organism.

            We see genotypic plasticity in conditions where adaptive-selective pressures favor certain features, characteristics or trait complexes in differential rates that are fairly discrete or continuous. If it is Darwin's finches--it may be in terms of fairly discrete differences of beak shape and size, or in terms of overall size of the individual bird, or in terms of a preference to sit in trees or stay on the ground, etc.

            Genotypical plasticity may itself be variable in an evolutionary or ecological context--shifting or shutting down under circumstances that favor other kinds of complex adjustments and adaptations. Many traits demonstrate a kind of evolutionary equilibrium and do not appear to quickly modify themselves. Human brains may have changed dramatically over the last two million years, but human dentition and human legs may have remained relatively unaltered by comparison.

            Any cell therefore may undergo evolutionary development. The whole of evolution was basically cellular evolution that was continuous from the first proto-karyotic cells until now. All life is cellular, and upon a basic cellular level, all life forms are interrelated. The cellular differences between organisms and organic structures are the most basic and greatest differences that exist in life. Evolutionary development of any cell involves a simple process of selection and reproduction of the cell, and its differentiation of DNA-RNA determined trait function and expression from one generation to the next.

            We may distinguish between intergenerational DNA differentiation that is controlled, presumably either self-controlled within the DNA (possibly cell life cycle) or controlled by other DNA (possible ontogenetic development) and DNA differentiation that is random and uncontrolled, or at least stochastically influenced by external environmental factors. Both kinds of DNA differentiation may be occurring at the same time.

No two cells are exactly alike unless they are cancerous clone cells, either in form or function, or in terms of their exact DNA structures. The intergenerational difference between any two successive cells may be only slight, but it may lead to substantial differences of structure and function in subsequent generations, over just just a few generations.

            If cells replicate every hour, on average, and life is estimated to be 3.5 billion years old, then we can estimate that since life began, there would have occurred more than 30, 660,000,000,000 cellular generations, during which time all the life as we know it and as it has occurred in the natural history record evolved. If we assigned a simple doubling time to the first organism, over generations, then we can speculate that there would have occurred a potential for a vast number of cells to have been formed (230, 660,000,000,000).

            If we see evolution occurring on an hourly schedule, rather than by the year or the century, the we can imagine that speciation may arise, under the right circumstances, as a function of days and months, rather than in terms of years and decades. Depending on the form of life we are dealing with, trait variation or its expression at least, may be delayed a very long time. We are talking about the exponential evolution of trait variation pattern at the cellular level.

 

Exponential Evolution

 

The natural history record proceeded in the beginning upon a long and low curved runway. For the first billion years, life was mostly constituted by rather simple forms of bacteria in interaction. How far these spread over the world is unknown--it is possible that they effectively spread via the oceans and even air transport to most surfaces of the range known now as the biosphere.

It appears that a major achievement was the rise of eukaryotic organisms with highly differentiated and compartmentalized internal structures, and many of these internal structures appear to have been based upon the incorporation of a cell by another cell, and either the transgenic or epigenetic transmission of new DNA information to the larger cell. The second step in this process was the deep invagination of the cell, possibly occurring at the same time as the penetration by a mitochondria or a cholorplast-type prokaryote, which led to the development of reticulated structures and the formation of a nulcear membrane within the cell. Early selection must have favored these secondary processes, as any deep invagination that is the result only of epigenetic information would be unlikely to be replicated by cell reproduction.

This poses an inherent dilemma, as it is difficult to simply explain many of the fundamental cell structures and functions merely by the invocation of DNA mutation, which process appears to be rather conservative and infrequent. It may also be the case that early protokaryotic cells lacked some of the backup mechanisms found in cells today that enabled DNA transcription to proceed without error--thus error rates for early cells may have been quite large. It is evident while most such errors would have resulted in cell death, a small percentage of the total mutations would have exerted a tremendous adaptive influence upon the first evolutionary stages of life. In such a context, every next cell was the potential progenitor of an entire Kingdom or phylum of life, and while cells eventually differentiated into distinct colony and family lines, a few such cells actually accomplished such success, perhaps against all odds. In this regard especially we must recognize that DNA as a molecule, and the entire transcription process of DNA to RNA to proteins, evolved also as a function of time. The protopathways that formed the basis for these later developments did not arrive on the scene full-blown.

            Thus, the first successful propagation of fully or partially eukaryotic lines, and their subsequent evolutionary development into more variegated and integrated structures, permitted the rise of multi-cellular organisms and many other associated features and properties, one consequence of which was the explosion of the diversity of life in all the major phylum still recognized today, less a few lost lines. This pattern exhibits the exponential character of evolutionary development, and of all living systems in general that have a fundamental doubling time at some relatively constant rate.

            We can only imagine the earlies proto-karyotic biosphere and its environmental ecology that enabled certain colonies and communities of these unicellular organisms to achieve long term equilibrium and the leap to proto-eukaryotic structures. Even after mass extinctions, what is recognizable is a long lag time, a period of delay, after which new life forms suddenly reemerge in yet another biological explosion of growth and development.

            We may state a basic principle of evolutionary development. For each evolutionary epoch that is marked at the culmination by a major extinction event, each epoch was ecologically dominated by the most advanced and differentiated life-forms that were then extant. The most evolutionarily advanced would be marked by the most differentiated biological structures, and would be the basis for an epochal exponential bloom of life.

            Overall, upon a cellular level, the conventional evolutionary model is stabilized by the conservative character of DNA reduplication. Subsequent processes of RNA transmission and transcription into complex protein structures are more inherently error-prone and hence variable than initial DNA replication, but these in general are not held to have any kind of evolutionary consequence except in directly by influencing the outcomes of natural selection for or against the cell. In other words, such post-DNA transcription errors would be a major source of genotypic variability and phenotypic plasticity of all living forms, but by itself it would not alter the basic DNA coding sequence to influence subsequent generations of the same cell line.

            The inherent accuracy and conservativeness of DNA transcription is in the conventional model regarded as the backbone for all evolutionary events. Variation is tolerated in RNA transcription, because it is evolutionarily inconsequential except in a negative sense of selection. But the question must be asked, in the evolution of living organisms, if living systems did not have some alternative means of achieving adaptive genetic variation more rapidly and more dramatically than what we have witnessed.

            Presumably, most post-DNA transcription errors would be either negative or neutral in effect, leading to loss of the cell.

            A case for indirect feedback can be made that positively selected alterations of post DNA coding errors might lead to a selective or stochastic advantage for these errors being repeated in subsequent generations, if alternatives are selectively eliminated and the DNA structures originally giving rise to these variations were positively influenced to reproduce at more rapid rates. Furthermore, selective advantage favoring a particular trait or phenotypical profile would possibly create an evolutionary framework encouraging greater selection for the trait complex thus expressed.

 

Only one mechanism that is suggested in this, but has not yet been documented and that goes against the fundamental tenant of the blindness of evolutionary process, is if there occurs any degree of feedback between protein and RNA encoded sequences and the original DNA that gives rise to these RNA. This may only be possible if RNA fragments might become spliced into, or somehow back-translate, to DNA sequences. So far, DNA to RNA to Protein transcription appears non-reciprocal.

            Several alternative processes might be invoked to explain radical reassembly or change of genotype in cell lines:

 

1. Transgenic insertion of alien DNA from a virus or bacterial infection: tranduction and transfection; plasmic conjugation

2. Reduplication of extra chromosomal complements, and the reorganization of these complements into new and active strands of DNA.

3. Accumulation of excess DNA material within the chromasomes.

5. Rearrangement of the same DNA sequencies into sub-sequences differently organized: i.e. transposition and recombination

6. Epigenetic transmission of information and or material structures, and the incorporation of such information or substance: transformation

 

Furthermore, proofreading mechanisms on a cell may not be correctly proof-read, at least in precursor structures, and may permit some inherent variability in the correction process itself. Such a mechanism would open up the process of DNA replication to much greater rates and degrees of variability than are otherwise permitted under the conventional model.

            Each or all or any combination of these processes may have been involved in one way or another, at one stage or another, in the evolutionary development of living forms. There are evolutionary phenomena at the molecular level that require sufficient explanation. These are the incorporation of mitochondria/cholorplasts into larger cell structures; formation of the nuclei and related reticulated structures; the rise of excessive and discrete chromasomal complements in cell progeny.

            We may distinguish possibly between old DNA and new DNA, from an evolutionary standpoint, and active DNA and inactive DNA, that may remain for the most part unexpressed in the organism that contains it. We might also distinguish what can be called as "basic DNA" that encodes those common structures shared by many organisms, or even universally, from "derivative DNA" that is a function of many episodes of evolutionary events, and that gets added to or inbetween the basic DNA complexes. We may speculate that derivative DNA is added on top of or inbetween basic, older DNA, possibly overpowering or swamping the expression of the older DNA, a form of cellular character displacement. We may also say, from observations of the natural history record, that older DNA may be less active or pronounced than the newer DNA that comes to take its place. It is evident that much primitive DNA is shared by many very different forms of life, which often gains expression in vestigial or ephemeral traits during early developmental periods, leading into the development of greater trait differentiation during later fetal or neonatal development. We may say that newer DNA may be more degenerate than older DNA, which may be more regenerate and more highly conserved.

            In a logical sense, if all of life is descended from a universal common ancestor, then a part of this ancestor's genetic code and the substances it encodes may well remain within ourselves upon a fundamental level. This would be found in every cell as perhaps the substrate of codon pairs in one or more basic chromosomes that would be more representative of most creatures on earth today.

            If all basic forms of eukaryotic phylogeny developed from a single period following the organization and formation of eukaryotes, then the precursor structures typical of these different phylogeny, particular between trophic levels such as producers, consumers and decomposers, must have been expressed in the variation of the proto-eukaryotic populations and in their subsequent ecological community organization, even upon a unicellular level long before the emergence of large and differentiated mult-cellulared organisms upon the planet. We can imagine in this proto-eukaryotic phase an ecological differentiation of function by different varieties of cells.

 

The basis of exponential evolution is the observation of the stability of a unimodal exponential growth curve of all living organisms. This pattern can be found in prokaryotic bacteria and free living eukaryotic forms, and it recurs at all levels of biological organization in multi-cellular lines, with the cloning functions of tissue cells traded-off for the survival of the organism as a whole. In a true analytical sense, multi-cellular organisms are nothing but a complex bundle of differentiated and specialized clone cells that have traded off their reproductive function for survival and growth of the organism as a whole, and entire populations of these multi-cellular organisms create larger evolutionary populations and breeding lines. Mechanical functions of cells becomes specialized and organized to the purposes of the systemic function of the organism of which they are a part, including such complex patterns as locomotion, environmental sensation and response, complicated neural networks leading to complex information processing, food getting and food-selecting behavior, etc.

            At any level of biological organization, it can be said that the pattern for population growth under favorable conditions will proceed exponentially at rates of generation time roughly proportional to the size of the organism, until that population achieves the maximum limits of its environmental carrying capacity. During this phase of exponential increase, it can be said as well that the degree of heterogenic, mutagenic and transgenic diversity will increase and be augmented to a maximum level. This can be referred to as the pre-selectional phase during which positive selectional factors relating to niche expansion and adaptation are more favorable than negative selection factors. The growth curve will taper off in a stationary phase which may be continued indefinitely if equilibrium of environmental adaptation can be achieved. This phase can be referred to as the medial-selectional phase during which both positiveand negative selection factors may be operating in some kind of complex dynamic equilibrium. Eventually, changing environmental conditions will result in the increase in the rates of death of the population such that rates of death will outpace rates of reproduction. This can be referred to as the post-selectional phase during which negative selection increases far above positive selection factors. Genetic diversity of a population will be bottleneccked during this phase, and, depending upon the predominating direction and types of selection occurring, certain specific phenotypic variants will be positively selected. At the point of lowest ebb of the population, at a point of greatest genetic bottleneck, which phase can also be prolonged indefinitely under some circumstances, the possibility of both extinction and of speciation becomes greatest. It can be said that in periods of bottleneck, rates of speciation from an evolutionary frame of reference are accelerated through the drastic reduction of variants. As a consequence, there occurs a niche vacuum, which may be either broad spectrumed or narrowly focused, within which there occurs ecological opportunity for new variants to adapt and achieve renewed population growth.

            In exponential evolution, the structure of this cyclical pattern of growth, development, stasis, decline and bottleneck are repeated over and over again. Each time the genetic constitution of the surviving populations being affected by such development becomes reshuffled and reorganized in new phenotypic patterns and genotypic templates. This patterning occurs at all levels of biological organization, and always occurs as well within a larger metabiotic context in which there can be said to be some kind of complex, dynamic equilibrium. What we get is a pattern of dynamic mosaic organization and succession of species in complex variegated biotic communities.

            The general picture of evolutinary development is that it proceeds in a step wise fashion, in a complex form of punctuated equilibrium during which phases of one kind of genetic diversification through population increase and exchange, is followed by other kinds of phases during which different selection regimes are operating upon a particular population. It is at the time when populations are declining that the likelihood of speciation becomes the greatest through bottleneck and subsequent founder effects. The likelihood of extinction can also be greatest at this phase. This brings to mind a picture of all populations of living organisms occupying some position along their own evolutionary curves, during which certain predictable kinds of outcomes may be determined for the group as a whole. These outcomes would dominate the lives of the individual members of the population as basic operating constraints. We may make the following kinds of observations:

 

1. Very small single celled organisms have very rapid and short-lived cycles and therefore depend upon mechanisms of rapid evolutionary development through short term ecological adaptation and global or regional distribution.

 

2. Very large multi-cellular organisms tend on average to have very slow and long-lived cycles, and therefore depend upon mechanisms of gradual evolutionary development through long term ecological adaptation and local distribution.

 

All living systems upon a cellular can be shown to proceed in biological growth and development in an exponential manner, until some upper limit eventually is reached by the cell growth, after which an extended stationary period follows, during which cell growth is in equilibrium with cell death, and at the final phase, cell death due to endo-proteolytic functions takes over. Multicellular organisms follow a very similar pattern of development.

It is evident that cells for instance have a number of genetic mechanisms of exchange and change available and that not all of these mechanism are bound by genomic reproduction and transmission. Cytoplasmic DNA may be replicated and transmitted outside of the cells nucleus. Various plasmids, mitochondria and ribosomes may contain DNA or RNA that functionally coexist outside of the nucleus and that may have a part to play in genetic development and evolution. Transgenic elements, particularly viruses, which are known to occur in all forms of living cells, and operate completely outside of the reproductive framework, also may have had an important influence in genetic development and evolution upon a cellular level. They appear to be able to confer upon cells certain adaptive properties during the cells lifetime, suggesting that organisms as a whole, and populations, may be genetically and phenotypically modified by these forms of extra-reproductive mechanisms. Phenotypic changes of multicellular organisms would not affect the reproductive genotype of these species unless the reproductive cells themselves became transinfected by extraneous DNA, but it does provide an environmental window for genotypic-phenotypic modification of post-reproductive organisms in a manner that can critically influence their survival. Furthermore, it is apparent that single celled organisms are not bound in this same way, and may acquire environmentally traits that can be readily passed on to subsequent generations as a normal functional part of their genetic machinery. The question naturally arises as to intermediate levels of organization occuring between single celled and multi-cellular organisms at which levels some kinds of process of environmental transgenesis may be occurring leading to evolutionary development.

Evolution upon a microscopic level proceeds exponentially. This exponential function is not just the result of r-selected forms of life that multiple quickly under suitable conditions. It is the result of relatively rapid doubling rates for uni-cellular organisms, and the capacity for such organisms therefore to quickly extend desirable genetic mutations through a population within a few generational periods. Rapid and sweeping trait-modifications can potentially occur within a short period of time within the exceptional circumstances, while gradual trait modification would be the normal rule under usual circumstances.

            The consideration of exponential evolutionary trends is based upon certain speculations about cellular structure and DNA structure in organisms over evolutionary time. If we observe trends of phyletic size increase and phyletic increase in differentiation and specialization of trait functions, then we must speculate about how this is reflected in terms of the DNA structure, composition and arrangement. We may speculate on the following kinds of hypotheticals:

 

1. In general, in evolutionary time, there is expected to be an increase in length of Chromosomal DNA segments that is reflective of phyletic size increase.

2. In general, in evolutionary time, there is expected to be an increase in the number of Chromosomal DNA segments that is reflective of phyletic increase in differentiation of trait function.

 

If this general model holds true, it can be expected for instance that mammals have on average more chromosomes than plants or reptiles, and that fish will have more chromosomes than algae. In all these instances, we are refering to eukaryotic cells where the chromosomal content is isolated in the nucleus in a form, exists in a haploidal DNA form, and where its transcription processes may be regulated and punctuated by one or more controls within the cell itself. What I wish to describe by this means in terms of evolution, is not the mere genetic mutation of chains, but the actual addition new genetic material to old chains. This appears to be a process that has been consistent with phyletic differentiation of species. The addition of new genetic material to a chromosome, or even of entire chromosomes to a nuclear structure, has not yet been described as a major contributory factor of evolutionary development, and how this may happen exactly remains a mystery. There are possible several alternative mechanisms for such increase in size and number of chromosomes:

 

1. Errors in normal transcription processes may result in added sequences to a chain, or else in the addition of multiple segments or chains as a whole.

2. Introduction of extraneous DNA material by some mechanism, as for instance by viral infection, or by symbiotic incorporation, such as may occur with primitive organisms, or that may occur in instances of sexual reproduction.

3. Addition or modification of RNA transcription chains that intermediate between successive DNA chains that may result in alternation of the final DNA coding sequence.

4. Point mutations in DNA or RNA sequences may result in repeat or repair structures being added to the DNA or RNA chain, with the result that point mutations may "drift" in their effect upon the genetic outcomes overall.

 

It may be that the structure of genetic encoding encourages repeat structures or sequences as a means of providing backup reliability in information transmission processes. It is possible that what emerged as a design to protect against errors or random point mutations, may have resulted in an accelerative trend in evolutionary development of organisms in the first place.

            It is apparent at the same time that many organisms may be carrying around more than a full complement of chromosomes, and that these chromosomes carry far more information than is actually necessary for the completion of the life-cycle of a single organism. Therefore, increase in size and amount of DNA over time, a process that cannot be accounted for by mutation alone, implies as well the likely accumulation of excess genetic material and hence a heavier genetic load than otherwise thought possible. It may be that relatively K-selected species in fact tend to carry a heavier than average chromosomal load, reducing the rates of transcription and transmission respectively.

            It is apparent that life may have evolved on basic levels the tendency to accumulate and gradually add to the DNA sequences that are the common thread of all life, but they did not evolve a complementary method for excising or removing excessive chains or segments from the system. It may be a kind of system that is so complex in terms of its interconnections, that an addition to a chain may or may not be deleterious or beneficial, but the removal of a segment would almost always assure a destructive or deleterious consequence to the cell or organism as a whole.

            It is also possible that some species may develop to a relatively high level of population saturation and increased K, and then back down the evolutionary period to a smaller size and more basic sense of production. Under such circumstances it would be expected that some genetic material that was once active and vital may suddenly become inactive and excessive. This excess code may not be excised away, but may only become deactivated and made dormant. We can expect therefore an gradual accumulation of archaic DNA structures, which structures may relate us as human beings back to the age of the Dinosaurs and before. We might see the role then of basic DNA structures that are shared between phylogenetically different organisms, on top of which are built different derivative sequences. Vestigial traits emerging and disappearing during ontogenetic development may be a reflection of such archaic DNA structures with a temporary influence upon the organism.

 

Such an accumulation of genetic material may result as well in the accumulation of "bad" DNA or dysfunctional sequences. In time, such accumulation may have negative effects upon trait development of organisms, and may even underlie the occurrence of sudden extinction of species in the fossil record.

            Another aspect of DNA structures is the built in presumption of a one-gene/one-trait correspondence, and a potential ignorance of the complexity of DNA informational processing in which different DNA sequences may be interlinked though not proximate at the same place or position within a larger strand. This may be especially true in multi-chromosomal structures, in which there is possible some kind of inter-DNA communication occurring, presumably in the form of a specialized RNA.

            Clearly, account has not been fully taken of the addition of DNA strings and sequences to the normal complement of cells, and it is apparent that this increase in number, size and complexity of such sequences may have been the basis for evolutionary differentiation in life. Such addition must have been gradual and rather slow in occurrence. Addition of DNA to the normal complement of a species would result in fundamental and radically pronounce acquisition of new trait patterns over time.

            The line drawn in the normal definition of species, that of reproductive success, may in some hybrid cases be blurred a little bit, if differences between mating pairs occur at a sub-species or even in a broader level. It is possible that, in closely related species or highly differentiated sub-species, that occassional interbreeding may result in the formation of entirely new species, on in a process that can be referred to as evolutionary amalgamation leading to the emergence of a new type. Distance in this case may be a matter of heterogeneous trait expression, as is commonly experienced.

On the other hand, there are also numerous examples of cases of prolonged in-breeding and the bottlenecking of populations to rather narrow margins of genetic variability. In such cases, the tendency for the expression of deleterious traits becomes marked, and the tendency for genetic maladaptability to changing environmental circumstances is also pronounced. Cases also appear of prolonged functional inbreeding as the result of small sizes of isolated populations or of functional sexual segregation in highly competitive environments, with similar kinds of results that can be expected. This kind of development may be expected for instance of highly K-selected creatures who have come to define for themselves very narrow and highly specialized niches and territories. In such circumstances the capacity for mating and mate choice may be narrowed so much that genetic variability over successive generations may be reduced. In such circumstances, high equilibrium would entail a sense of long-term stability that would be conducive to intergenerational patterns of breeding.

            The picture that is being painted in terms that I refer to as exponential evolution is that though the total genetic informational complement for an organism may have a fairly broad base, the margin for expression and continuity of a genetic type may be in the long run quite narrow, such that it can tend toward rapid phyletic differentiation in adaptation, or possibly towards sudden and deleterious expression of mutations and defects that are normally kept silent. Creatures may exhibit in this regard fairly robust and broad-based adaptations, but there is a limit either in terms of adaptability or dysfunction beyond which the entire genetic system of a population may loose its equilibrium and fall into a condition of general disequilibrium.

            To expound a basic set of postulates for exponential evolution, we may make the following statements:

 

1. Phyletic increase in size and differentiation of function is reflective of the increase in size and number of DNA sequences involved in the transmission processes of a kind of organism.

 

2. Increase in number of DNA must therefore be a major factor in evolutionary differentiation and development of species, as both a compensatory factor for the random rise of deleterious sequences and DNA, and as just a normal process of increasing genetic load.

 

3. Addition of genetic material may be both deleterious and beneficial, and is usually deleterious in the long run.

 

4. Genetic encoding becomes more complex in terms of its intensive differentiation and interconnection of function, as well as more extensively developed.

 

5. The gradual increase in DNA size, amount and the ensuing genetic load tends to alter species from an r-type toward a K-type mode of development and adaptation, and can be expected to arise as a result of K-type selection factors.

 

6. A supercritical point will be reached in loading of DNA such that the system becomes informationally noisy and possibly breaks down in its capacity to confer trait adaptability to a species or type of organism, as a result of which extinction can be expected, especially in a context when such a heavy genetic load may intefere with an organisms ability to become more r-adapted to changing circumstances. This would be evident in lower rates of fertilization, conception and successful births, as well as more frequent cases of immature organisms failing to develop properly to mature reproductive form.

 

7. In the long run, additive process to DNA seem to occur far more frequently, at a much greater rate, than deletive processes. This entails that deletive processes in the fossil record are probably unusual and exceptional. Deletion of DNA from gene pools probably takes the form of negative selection that favors lower loads of variability between individuals.

 

From the standpoint of this theory, the rise of haploidy in chromosomes represented a major development. Sexual reproduction guaranteed a kind of metabiotic dependency for transmission on other organisms, and that each cell would normally carry a double complement of genetic information. We know from gene studies that for every trait or trait complex there will be two alleles that are possibly represented. We do not yet understand the mechanisms involved that assures the dominance of expression of one allele over the recessive counterpart. It is possible that more than one kind of recessive or dominant allele can occur in multi-trait systems. Haploidy may have assured a backup system in case of error in genetic coding sequences, and it may also have provided a basis by which genes had to be regularly exchanged between organisms to prevent or at least forestall perhaps the rise of monogenetic trait systems. It may have provided as well a context within which DNA had a basis for additive accumulation in a manner that may have minimized the deleterious effect of such processes. Haploidal systems comprise in general a greater range of trait variability that would enable such systems to better adapt through population growth, given that such systems are in a fundamental sense, when compared to more primitive bacteria, in general slower to reproduce and more complex in their organizational structure. Haploidy therefore may have provided the platform of builtin intergenerational genetic variation to enable more complex trait-systems to be developed. It certain provided the frame work for an inherent increase in the number of genes available to do the work. Haploidy leads into polyploidal systems, and polyploidy has also been observed to occur in a limited number of cases that are to be considered aberrant.

            The kind of system we see is a long term evolutionary advantage to increased trait systems of DNA, and to the inherent variability these systems afford in terms of trait-differentiation and adaptation, even at the expense of short term stability or deleteriousness of carrying a heavy genetic load. This works as a kind of cybernetic feedback system such that increasing DNA structure increases adaptability, which in turn may foster conditions leading to further addition of DNA.

            The gradual accretion and organization of DNA is simply accountable in terms of the basic biochemical processes that occur in the construction of DNA in the first place--it is possible that the signals that shut down the construction of DNA may result in the addition of more DNA material than is normally required or encoded for. DNA construction may on occasion fail to stop or go into a kind of overdrive that results in a kind of experimentation of the system through systematic variation. Cancer cells would represent one kind of DNA transcription system that has gone awry, leading to the continuous replication of new cells, but without genetic variation.

            This theory is based upon a very fundamental premise about basic biological variability. It can be summarized thus:

 

Every living cell that is produced as the product of cellular division, is biochemically unique in its overall trait-properties.

 

No two cells, however related, are exactly identical to one another. All cells have a degree of variation within which they can achieve expression, and this variation occurs within the framework of the cell's membranes and internal structure, as well as in its DNA encoding. What I will call as inherent fundamental variability is really the basis for all variation of pattern and evolutionary change in living forms. It provides the basis for the successive cellular differentiation of cells within some developing tissue matrix that results in the eventual differentiation and specialization of cell function in multi-cellular organisms. This variation is continuous and occurs at a continuous rate, and can be accounted for by the shear bio-chemical and macro-molecular complexity observed within all cellular life-forms. Cells, as heterogenous, enzyme based rate systems, depend upon speed of reactions within a very small area in order to accomplish their metabolic and growth/reproductive functions.

 

Inherent fundamental variability of cellular systems is the basis for the biological relativity of living systems and for evolutionary irreversibility of such systems through time. It assures that changes will occur in an historically forward direction, as once new systems emerge, they will continue to vary, and will not return to the state of previous systems.

            We can therefore understand those few very conservative systems in nature that appear to change very slowly. They must exhibit a system in which inherent fundamental variability, and its integrative, chaotic effects in mature organisms, is kept in check and minimized. The mechanism of control in this case may be an narrow adaptive equilibrium that assures a minimization of genetic load and the selective elimination of any strong variants. This may be reinforced sexual by built in systems of preference that serve to minimize the crossing of heterozygous forms and that may lead to a long crane-like bottlenecking of genetic variability represented by such species.

            Genetic addition can be seen therefore as a buil-in function of systems of DNA production and replication in which the processes of DNA transcription and replication are decoupled from the processes of other cellular metabolism, growth and reproduction, and in which case control mechanisms exist that may permit the accumulation of excess DNA without deleterious effects upon the functioning of the cell, or even in its reproductive phase. Such systems are clearly represented by the eukaryotic domain, and they are represented essentially by the incorporation of prokaryotic forms, chloroplasts and mitochondria, as internalized forms. It is possible that the DNA from these prokaryotic subunits was contributed to the DNA of the enlarged proto-eukaryotic cell to enable a platform for greater differentiation of form and function than was otherwise possible.

            This may also have set the stage for multi-cellular organization of increasingly more complex systems. Such systems are represented by shared inheritance of a single complex of DNA trait material that controls the differential growth and function of all the cells with each successive generation. The cells of such a system yield reproductive function, and usually motility, in order to enhance the productive function of the system as a whole--they gain from this an environment that is minimal optimal and suitable to their survival. That reproductive function must be yielded to increase the potential for social organization is a principle that was not lost upon social insects, and it appears to be an important emerging concern for oversaturated human populations as well. Human systems have accomplished this by the superimposition of monogamy, or alternative the alpha predominance of indivduals who are exclusively polygamous. Further increase in human population is creating a demand for further control of human reproduction to monoparous families.

The rise of multi-cellular systems again can be seen as having been made possible by the functional segregation of sexual reproductive function from normal cellular metabolism, growth and division replacement, which was the product of separating processes of DNA encoding and replication from the encoding and replication of the cell body itself. In such a context, generations of cells stemming from the same parent generation can be increasingly organized in such a way that some cells carry reproductive functions selectively on behalf of the entire cellular community, while other cells provide other functional roles in the organization of the community structure.

            It can be seen that DNA transcription may therefore result in a systematically changing genetic structure through time for successive generations of these organized cells, such that specialized functions of select cells become increasingly expressed by the subsequent copies of the DNA. This is possible if we conceive that in a DNA detached system, the RNA transcription process may introduce regular and systematic variations of structural encoding at regular intervals. Again, as mentioned previously, this may be the result of a master or controlling DNA, or of built-in pathways within the genetic coding itself, or by some genetic signaling system we do not yet understand, or else by the common environment or emerging tissue matrix in which the cell itself is embedded. In this regard, a base stem cell may become differentiated in its growth in any number of alternative directions depending upon the biochemical nutrient base and other properties made available to it. Hormones, steroids and certain kinds of enzymes in combination appear to me to be particularly implicatable in such differentiation processes. Such biochemical signals may stimulate and activate the transcription of some genetic sequences, and repress or deactivate the transcription of other alternative sequences simultaneously. These reactions would all occur within the context of the cell itself, and in the exo-cellular tissue environment in relation to other cells. Cells may in this regard be exchanging chemical signals in a regular and influential manner. We may speak of possible regulator sites in chromosomal complexes, in organelles, as well as in cell tissue complexes that serve to control the formation and development of cell tissue patterns and functions. Such a prospect suggests something fundamental about genetic systems, that genetic systems of one cell may have a metabiotic and adaptational influence upon the systems of other cells, even possibly affecting the differential expression of genetic traits.

            This suggests in turn that genetic chromosomal systems may in fact be communication systems that exhibit a duality of patterning, or even a multiplicity of patterning, that allows the same genetic sequences to be used in fundamentally different ways within different complex arrangements. Folding structures may be the basis for these kinds of systematic differences. Duality of patterning suggests that all traits complexes are both pleiotrophic and polygenic in nature. How the same chromosomal structure may be used to different purposes remains an unanswered mystery. We see a translational structure in successive translation of genetic sequences leading to different forms and functions of the same basic genetic material.

            It must be understood in this that genes control exclusively the cellular structure and function of the cell body they inhabit, and they control the transcription process to the next generation of cells. Therefore, however we describe genetic function within a cell, it must be in strict terms of the metabolism and organization of the cell itself. DNA does not work remotely between cells in any direct manner. They function only in terms of the cell that it is situated in, and indirectly upon cells that are near it or that are functionally related, and those cells that it gives rise to through growth and reproduction. That some of these functions may take on extrasomatic properties in relation to other cells is a moot but not unimportant point. A gene that confers, for instance, color to hair, must find expression in the cells that produce the hair follicle, and not in the cells that produce toenail in the big toe. The gene that produces the hair follicle may be the same gene found in the big toe, only differently expressed in combination to other genes. DNA structures must differentiate in the process of ontogenetic growth, just as they do in evolutionary processes of speciation.

            Genetic complexes can be seen therefore to control trait-complexes in sophisticated ways. That folding structures of genetic material, with the secondary bond formations that occur, may be important in the organization of these complexes and in influencing epigenetic trait expression.

            It is doubtful in this regard that we could take the genetic material from a skin cell in the tip of the big toe, and inject it into the egg cell, and from it derive a replica of the same person who was attached to the big toe. The organizational structure of the DNA in the big toe may not be exactly the same or of the same organizational structure as that in the

DNA is not passed wholly from one generation to the next--it is transcribed and translated afresh with each new generation. The reproductive growth of cells represents a fundamental exponential increase in the total amount of DNA material that is being encoded and used in all of the cells. We may refer therefore to ontogenetic life-cycles of DNA development, differentiation and increasing elaboration from basic and source code to derivative and end-code. In this regard, the rate of DNA replication must be synchronized with the growth of tissue, such that once tissue has reached its stage of full development, growth is switched over to a slower rate of repair and replacement. External limiting factors may fundamentally control these processes, with mature cells obtaining a kind of equilibrium of internalized community structure that represents a saturated cellular system.

            With these processes of continuous and successive transcription of DNA, multiple occassions arise in which the average amount of DNA available to a cell may increase through transcription itself. In other words, DNA is continously replicating itself, thus providing the basis for production of excessive code. It is in this production of excessive code that the possibilities for variation and evolution arise. It is possible that even within cell tissues of an organism, genetic material may slowly accumulate in successive generations, which accumulation may have a critical effect in the regulation and timing of metabolic and reproductive growth functions. In this, the growth of any tissue would therefore be seen to follow a normal unimodal growth curve that is very flat. Each successive generation of cell would represent an instantaneous point upon this growth curve. The slope of this curve at any point is quite variable between different kinds of species, and the time required for an organism to reach full maturity may vary from days to months to years or even decades. Cell tissue in old-age would eventually break down in function and structural integrity by the exhaustion of a DNA complex systems that has reached a stage of supercritical chaos in its organization.

            The received model of DNA structure is that it is a fairly stable backbone of life. The transcription process is inherently stable, with back up mechanisms to safeguard against error. DNA transcription in eukaryotic life forms passes to messenger RNA as a single large strand. The sequences are linearly encoded with segments of introns. The messenger RNA is then broken down into its sequential units, and transported outside of the cell to ribosomes where it is translated into transport RNA, which RNA then manufacture the protein chain encoded in the sequence. It is the proteins that show the greatest variability of form and structure, and the shape of protein molecules will be critical to determining its enzymatic function and the resulting geometric structure that cell tissue will take. The variability that is demonstrated in life upon a fundamental level is best expressed at the stage of the folding structures of the protein molecules, and the larger structures these molecules form. These sequences are discretely determined by the precise DNA coding sequences. It is known that point mutations occur in DNA sequences with regular frequencies, and there are recording errors in the transcription process as well that may result in mishapen end products down the line. DNA sequences can be spliced and juxtaposed. There appears possibly to occur room for variation in the second stage of the slicing up of the mRNA and its transport and transcription back to tRNA. The disassembly of the starter mRNA might result in alteration of sequences.

            The entire problem of evolution can be described upon a microscopic level in terms of the process of DNA transcription through RNA sequences in the production of a vast array of different kinds of proteins that constitute the true building blocks of life. Selection will be determined by cell death or by its ability to survive alterations, and by its ability to confer adaptive advantage to the organism of which it is a part.

In the diagram above, we can see the multiple steps involved in the sequence of cellular actions that result ultimately in the outcome of cellular demise or reproductive success. With each step, the degree of variability of pattern becomes magnified exponentially. At the same time, with each successive step, the potential for error pattern to arise randomly and for its effects to become pronounced magnifies exponentially as well.

 

1. Random changes that occur in more basic and earlier steps are likely to have more pronounced and generalized consequences.

2. Random changes that occur in the final steps of the process are less likely to have major or pronounced effects, and will only affect specific protein molecules.

 

Previous to the final step, it is possible that what I call endo-somatic factors may play a part in determine the structural and functional outcomes of the process. In the final step, it is apparent that extrasomatic factors will play a decisive part in determining the outcomes for the continuation of the cell line. These factors may be independent of endosomatic factors or resulting structures, for instance, chance death of an organism due to some natural disaster. It is expected that the majority of mutation events are likely to be either negative or neutral in their evolutionary effects, and this can be accounted for by the fossil record that suggests that the vast majority of life forms eventually became extinct. Neutral build up of genetic mutations are likely to have in the long run a negative effect upon the subsequent population as a whole, but may confer a wider range of adaptability to a select number of offspring.

            It is evident that there are entire families of proteins that share amino acid sequences in a non-random manner and that indicate some measure of genetic relationship and common inheritance of structure. The repertoire of protein structures and functions has evolved in time, as have the necessary genetic precursors--the DNA sequences, that determine these protein structures. The pattern observed in protein sequence coding of related proteins, indirectly reveals patterns of change that occur in the underlying DNA sequences.

            Regardless of this, it is apparent that DNA change is the basis of evolutionary development. Though the greatest genetic variability is found in terms of the folding structures of proteins, and their derivative structures, it is clear that the basis for variability of these structures begins with the DNA material itself. DNA material must exhibit a minimal degree of variability in coding sequences. It is evident for instance that point mutation may result in the attempt of the DNA strand to repair itself not by the excision of the mutated component, but by the addition of more components that correct for the coding error and possibly mask this error. Haploid sets of genes may have been a device for the protection against random genetic mutuation, which effects might result in the suppression of the traits encoded, and the activation of the complementary set of genes that are tied to the same trait complex.

            It is apparent that genetic mutations must build up over time upon a single chromosome, and that eventually this will result in this chromosome having a fundamentally different set of sequences than the complementary one. It is known that all chromosomes come in sets of two, and that all chomosomes are whole. There are never half or quarter chromosomes in organisms. This suggests that at some point, differentiated pairs of chromosomes may in fact separate from one another and become replicated as two independent sets. Separate chromosomes will differentiate more and more as a function of time. The alternative is that a chromosome may grow in size and sequence length until it becomes divided into two separate and independent strands, or becomes divisible by some mechanism.

            To what extent must chromosomal variation of gene sequence occur before the resulting organisms are biologically separate from their progenitors is unknown. Presumably it does not require too much difference for this to occur. The fact that this variation occurs only in the sperm and egg cell constrains the model somewhat, except that we must realize that new sperm and egg cells are being produced or exist via mature sexual organs within the body. This provides a pathway within the context of the larger organism for the occurrence of further genetic mutation that may have a direct evolutionary consequence. Mutations occurring in toe-cells are not likely to have the same evolutionary effect.

Most mutations are probably deleterious in the long run, but continuous mutation and transcription error will create changes in protein structures that will open the door to the possibility of non-deleterious or even beneficial changes to happen. The amazing trait plasticity of living forms, evidenced by so many different kinds of organisms that seem so well streamlined and adapted to their main host environments, is accountable for purely in terms of this protein variability that is the result of a number of different mechanisms possibly occurring at the same time.

            The question to be answered is to what extent must DNA material become altered before there can be said to occur speciation and reproductive isolation between two or more organisms. In this context, with multicellular organisms, the alterations must affect only the DNA material located within the sexual gametes of the parents. The mutation of genetic materials in other cell components of the parent organism may indirectly affect the survival of the organism, but these factors will not be replicated or become expressed in the genotypes of the offspring. One of the trade-offs in terms of controlled reproduction for muli-cellular organisms is that the generation time between reproduction at which time evolutionary changes can be expressed becomes extended over considerable periods of time, and in general loses its exponential growth function. As length of generation time increases, the rate of evolutionary development must slow down accordingly. There must be a corresponding increase in the potential for genetic variation in larger, more differentiated organisms, that is due to the larger complement of genes necessary for encoding and for their slower rates of replication, but this is perhaps balanced by the confinement of reproductive cells to specialized classes.

            It is evident that there occurs phyletic increase in the size and number of chromosomes available for sexual reproduction. In this case, we see no "half" units. We find in the sexually reproductive world only paired sets that occur in discrete numbers.

 

Exponential Evolution, DNA-Insertion, RNA Back-Translation, Viral Addition and Polyploidal Differentiation of Eukaria

 

The basis for the argument of exponential evolution is the idea that mutation mechanisms alone, that tend to be conservative, cannot explain by itself a fundamental feature of evolutionary divergence, and that is the enlargement of the chromosomal complement of the genome with increasing speciation. Other unknown mechanisms must be invoked to explain this increase in gene numbers besides mutation rates or even simple transpositions. Both these mechanisms describe how genes differentiate on a fundamental level, but not how they accumulate or increase in number. I propose a list of viable candidates, all but one of which are based upon empirically described mechanisms that normally occur in cells, or that are known to have occurred in cells during their evolutionary development from prokaryots to eukaria. These mechanisms are listed below:

 

1. DNA Insertion: Extraneous DNA from other microbes, or from organelles in the cell known to contain DNA, become incorporated at some stage into the genome of the nucleus of the cell and become a permanent part of the DNA structure, either as a whole structure, or as segmentable substructures that could be variably incorporated into already preexisting DNA molecules.

 

2. RNA Back Translation: This is only a hypothetical pathway that suggests that foreign RNA might somehow become involved in a process of back-translation of DNA, as is known to occur, for instances, in the life-cycles of retroviruses.

 

3. Viral Addition: Viruses are known to carry a DNA or RNA complement that can be inserted systematically into a cell nucleus or into its relevant ribosomal RNA structures, and there be incorporated into the normal complement. It is possible that in certain instances, such inserted strands may become a permanent part of the DNA strand of the host cell, thereby fundamentally augmenting the number of DNA. A chance mutation of such a strand in the process of insertion or during its period of insertion may affect the subsequent function and recognition of the insertion.

 

4. Polyploidal Differentiation: This theory suggests that polyploidal is a natural consequence of chromosomal replication that leads to the formation of multiple pairs of chromosomes, which may or may not be active within the genome, but which would subsequently diverge and differentiate in terms of mutation and transposition of available elements. Polyploidy can be explained in terms of the ability of cells to withstand high rates of genetic mutation, providing "back up" copies of genes that can be "turned on" in the case of genetic failure of the master gene.

 

Two other sets of pathways must be suggested in this process. The first is some combination of any or all of the pathways above, and the second is some combination of any of these pathways with or of unknown and as yet undescribed pathways employing other kinds of mechanisms of genetic alteration.

 

 


Blanket Copyright, Hugh M. Lewis, 2005. Use of this text governed by fair use policy--permission to make copies of this text is granted for purposes of research and non-profit instruction only.

Last Updated: 08/25/09