| Morphological Flows and Sustainable Growth : Evolutionary Philosophy - where we came from and where we might be headed - NAVIGATOR-->Part A-Morphological Flows: -Introduction- Creation of Matter {1-Particles--> 2-Atoms --> 3-Molecules --> 4-Proto-Biota}--> Creation of Life { 5-Biomolecular (Genetic) mechanisms --> Tree of Life, Fossil Record and Comparative Anatomy { 6.1-Cells to Reptiles --> 6.2-Reptiles To Man --> 7-Nervous System and Brain } --> Creation of Us {8-Behavioral Evolution --> 9-Social/Cultural Evolution} -- 10-Segue: Common (Cascade) Model for Morphological Flows -->Part B- Application of Flow Oriented Analysis: Sustainable Growth {11-Exponential Population Growth -->12- Exponential Demand Growth --> 13-Social Rifts --> 14-Solutions for Sustainability} --> Fun Stuff {15-Attractor sets and Turn-ons List --> 16-Intellectual Attractor Sets} ----------HOME---------- (c) contact Mike Baharmast - MBScientific |
1- Historical Perspective - Manmade Natural Selection
and the Evolution of Genetics
2- Gene Structures, Genetic Networks and the Shape of Life
3- Evolution: Design Driven or Accidental?
4- Natural Selection and Genetic Evolution
1- Historical Perspective - Manmade Natural Selection and the Evolution of Genetics
Probably the most direct evidence of biotic
morphogenesis in
action is our own breeding experiences with animals and crops. Lets
start with crops. Our agricultural experimentation started some 10,000
years ago in Mesopotamia and later on elsewhere, either independently
or through diffusion. Inevitably in all cases, after each planting
season the seed varieties that yielded the desired quantity and quality
where selected for the next planting season. Generation after
generation, this selective breeding has yielded strains of wheat, corn,
rice etc., that are substantially different from their wild varieties,
and better suited for consumption, both qualitatively and
quantitatively. Your store bought corn, for example, is far bigger than
the wild variety.
Selective breeding has demonstrated morphogenesis in animals as well.
Dogs, cats, horses and other livestock have similarly gone through
significant transformation. Dogs vary from teacup sized Chihuahuas to
enormous Great Danes. Horses vary from toy ponies to massive
Clydesdales. One could compare the results of human driven selective
breeding to nature driven selective evolution. If you look at
variations in the sizes of rodents, say from mice to rats to Capybaras
and compare it to the size variation in dogs, for example, the
similarities are glaring.
From a scientific perspective, the table below lays out the landmarks in the history of genetics (source: http://cogweb.ucla.edu/EP/DNA_history.html):
Year |
|
Theoretical implications |
1745 |
Maupertuis proposes an adaptationist account of organic design |
Presupposes some mechanism for transmitting adaptations |
1859 |
Darwin publishes The Origin of Species, vastly strengthening the adaptationist hypothesis |
|
1865 |
Gregory Mendel publishes evidence for the discreteness and combinatorial rules of inherited traits |
Traits are carried by discrete units, or genes; the results are not appreciated until 1900 |
1869 |
Miescher discovers "nuclein" (DNA) in the cells from pus in open wounds -- cells composed mostly of nuclear material. It became known as nucleic acid after 1874, when Miescher separated it into a protein and an acid molecule. |
Suspected of exerting some function in the hereditary process |
1918-1926 |
Muller formulates the chief principles of spontaneous gene mutation as point effects of ultramicroscopic physico-chemical accidents; he induces such changes using X-rays |
The gene constitutes the basis of life and evolution by virtue of its property of reproducing its own internal changes |
1920s |
Nucleic acid found to be a major component of the chromosomes |
Its molecular structure was thought to be simple, so it was not a good candidate for a carrier of genetic information |
1930s |
Chemical nature of nuclei acid investigated. It was thought to be a tetranucleotide composed of one unit each of adenylic, guanylic, thymidylic and cytidylic acids |
The ubiquitous presence of nucleic acid in the chromosome was generally explained in purely physiological or structural terms |
early
|
The molecular weight of nucleic acid was found to be much higher than the tetranucleotide hypothesis required, but it was still viewed as a uniform polymer, like starch, unaffected by its biological source |
Hereditary information was commonly thought to reside in the chromosomal proteins, since these differ across species, between individuals, and even within an organism |
1944 |
Oswald Avery identifies nucleic acids as the active principle in bacterial transformation |
"If the results of the present study of the transforming principle are confirmed, then nucleic acids must be regarded as possessing biological specificity the chemical basis of which is as yet undetermined." |
1950 |
Erwin Chargaff shows that the four nucleotides are not present in nucleic acids in stable proportions, and that the nucleotide composition differs according to its biological source. |
The nucleic acids are not monotonous polymers. |
1952 |
Alfred Hershey and Martha Chase show that on infection of the host bacterium by a virus, at least 80% of the viral DNA enters the cell and at least 80% of the viral protein remains outside. |
DNA rather than proteins carry genetic information. |
1953 |
Watson and Crick determine that deoxyribonucleic acid (DNA) is a double-strand helix of nucleotides. Each nucleotide consists of a deoxyribose sugar molecule to which is attached a phosphate group and one of four nitrogenous bases: two purines (A- adenine and G- guanine) and two pyrimidines (C- cytosine and T- thymine). The nucleotides are joined together by covalent bonds between the phosphate of one nucleotide and the sugar of the next, forming a phosphate-sugar backbone from which the nitrogenous bases protrude. The two strands are linked by selective hydrogen bonds: the purine adenine bonds only with the pyrimidine thymine, and the purine cytosine only with the pyrimidine guanine. |
DNA replication is possible through the complementary nature of the two strands. The chemical complexity of the molecule is thought to be sufficient to store the requisite information. The precise manner in which the information in the DNA is activated to build an organism is still very poorly understood; what is firmly demonstrated is that so-called structural genes manufacture the proteins for living tissues. |
Early 1970s |
Comparisons between chimpanzee and human genomes finds that they diverge by only 1.6%--less than most sibling species, which barely differ in morphology, and far less than that between any pair of congeneric species (Wilson 1975: 113) |
The theoretical implications are unclear; morphological and behavioral differences between the two species appeared to be unaccounted for by the genetic material (cf. Cherry et al, 1978; for an update, see Gibbons 1998). |
Early 1970s |
The discovery of regulator genes--genes that control the timing and output of structural genes |
Since a regulator gene may control thousands of structural genes, and indeed other regulator genes, the logical inference is that human and chimpanzee genomes are being switched on and off in quite different ways (King and Wilson 1975) |
1980s |
McClintock discovered transposable strands of genes in maize already in the 1940s, but her work was not fully recognized for a generation. |
The genome may be controlling aspects of its own mutation (see Pennisi 1998 and Chicurel 2001 for an overview). |
1984 |
McGinnis discovers homeotic (Hox) regulatory genes, responsible for the basic body plan of most animals. In subsequent work, his team demonstrates that a single mutation in a Hox gene suffices to suppress all limb development in the thoracic region of fruit flies. |
Macroevolutionary transitions, such as that from arthropods to hexapods (insects), may be initiated by point changes in regulatory genes. |
2000 |
The Human Genome Project presents its preliminary results: each of the body's 100 trillion cells contains some 3.1 billion nucleotide units. Only 1% of these are thought to be transcriptional, clustered in possibly as few as 30,000 genes. |
An accurate chemical map of the genome tells us surprisingly little about how it functions. Targeted experimentation is now possible. |
2- Gene Structures, Genetic Networks and
the Shape of Life
The figure below demonstrates DNA structure:
DNA consists of coding parts (exons) and non-coding parts (introns). One of the jobs of DNA is to make proteins that do all of the cell's functional work, including determining what a cell will be. To put things in context, shapes form as cells divide and differentiate. The fertilized egg (zygote) divides into a bunch of undifferentiated cells in a uniform clump called blastula. During gastrulation, when cell differentiation occurs, three major cell lineages are established. They are the Ectoderm (shown in the diagram in blue), Mesoderm (red) and Endoderm (yellow). Following gastrulation, various cell lineages are derived from these three primary cell types. For example, the Ectoderm gives rise to the epidermis and its derivatives such as nails, hair and teeth. The cascade looks like (source: http://www.luc.edu/depts/biology/dev/devm.htm):
At each step a number of genes are deactivated and a number of genes activated. The expressions (i.e. the work) of the activated genes determine what proteins are created and therefore what the cell will be. The chart below establishes a typical number of proteins in the cells of several different species (source: www.nature.com, article on human genome project):
DNA doesn't produce the proteins directly. Rather, DNA is transcribed to messenger RNA (mRNA), which strips out the introns, leaving only the functional exons. It is the mRNA that codes the proteins. Given that relationship, we can potentially tell what segments of the DNA, i.e. genes, are responsible for the manufacturing of what proteins. And, given the functionality of a given protein, we can deduce what gene is responsible for what functionality. Relationship between codons (3 letter slice of DNA) and the amino-acids (protein units) they code for is given below:
Legend: Amino acids specified by each codon sequence on mRNA. Key for the above table:
Ala: Alanine |
Cys: Cysteine |
Asp: Aspartic acid |
Glu: Glutamic acid |
Phe: Phenylalanine |
Gly: Glycine |
His: Histidine |
Ile: Isoleucine |
Lys: Lysine |
Leu: Leucine |
Met: Methionine |
Asn: Asparagine |
Pro: Proline |
Gln: Glutamine |
Arg: Arginine |
Ser: Serine |
Thr: Threonine |
Val: Valine |
Trp: Tryptophane |
Tyr: Tyrosisne |
A = adenine G = guanine C = cytosine T = thymine U = uracil
In the ribosome mRNA codons produce the aminoacids which are then chained together to make the functional proteins. In the last chapter, we defined 5 major call functions (structural, replicative, metabolic, motor/sensory, signaling) and elluded to biotic aggregates that manifest these major functions (a more complete list of functions are spelled out in the cell protein chart above). Now we know what these aggregates are: DNA-tRNA-mRNA-Proteins.
Again, during differentiation, the activated genes and the proteins they produce give rise to the identity and the functionality of the cells. The genetic network that successively activates and deactivates various genes as the cells divide is the mechanism of cellular differentiation, as the cascade below demonstrates:
So you can look at DNA as a series of time-lapsed functional and regulatory networks. The functional parts make functional proteins and the regulatory parts make regulatory proteins that become hierarchically activated at various stages of cellular differentiation (body formation). I'm going to include a gene network model for endoderm-mesoderm differentiation (without explaining it, otherwise we'll be here for a month- source: http://www.its.caltech.edu/~mirsky/endomes.htm):
Presently the sequences of the genomes of humans, mice, various bacteria and viruses have been completed. Further DNA sequencing work is continuing on a variety of species under study. In a nutshell, we are approaching an era where we can study biotic morphogenesis from an elemental, genetic angle. For example if we suspect that two species are related, because of morphological and behavioral similarities (e.g. man and chimpanzee), we can compare their genetic sequences (man and chimp have ~%99 common genes) or the protein sequences that genes produce and arrive at a quantitative measure to express their similarities.
3- Evolution: Design Driven or
Accidental?
This would be a good point to try to answer the primal
question: is biotic morphogenesis driven by design
or is it accidental?
Part of the problem is the way the question is posed as an either-or.
Let's set the context and maybe that'll help. There maybe valid states
that things can evolve to. But the valid state doesn't force the
evolutionary process. Rather, it seems, the evolutionary process starts
with the initial valid state and tinkers with it. Through the
generations this tinkering happens over and over. It isn't accidental.
It is driven by the biomolecular machinery, but it radiates in all
kinds of directions and not necessarily only towards the valid state.
With luck one of the directions of radiation actually points toward the
valid state. The main problem with the valid state is that you don't
know what it is before hand. Rather, it is something that emerges as
the result of the evolutionary process. Take the emergence of animals
out of water and onto land. Now we know that the bipedal morphology is
a valid design. But the question asks whether the original fish design
drove towards the bipedal state by some design or did it accidentally
get there. The answer is both. We know lobed-fin fish probably evolved from ray
finned fish. The lobes at the base of the fins provided the muscles
that stand out from the flimsy fin bases of ray finned fish. And, when
we look at the swimming motion of the living fossil, the coelacanth, we
see a bipedal type of motion. But, the coelacanth is a creature of deep
oceans. It doesn't come anywhere near land. The next cascades of
evolution moved the lobed fish valid state in all manners of
directions. One was the direction where the fin bone structure gets
thicker and sturdier. That adaptation was useful for the fish that
inhabited swamps. It allowed them to maneuver in between the trees and
roots and avoid their predators. So they established that niche. The
next evolutionary step would be conversion of fish air sacs to lungs,
as in the lungfish. The creatures that combined these two traits
happened to have the right tools to move about on land. The ones who
managed to survive struck their niche on the shores. So the first
amphibians were established. But they didn't just establish by
themselves. The entire shoreline eco-system had to emerge along with
the amphibians, otherwise there would have been no place for them to
establish a niche in. So the evolutionary process has to involve the
whole system. And only in the context of the whole system you can tell
a valid state, and you know it because it has already been established.
You wouldn't know it before hand. This is a perfect example of
emergence of valid states from chaotic morphological flows, as has been
evident throughout this exercise.
4- Natural Selection and Genetic Evolution.
Let's look at the tree of life from a lineage standpoint. You'll get a more detailed tree made up of actual individuals that make up the physical nodes that make up the tree of life (w=female, m=male).
One can see that a beneficial genetic mutation would potentially get inherited by the successive generations and establish a noticeable morphological change. But there's more to the picture though. You can also construct an upside down tree, consisting of all the different individuals through one's lineage that could contribute to its genetic makeup:
So one's genetic make up can consist of a wide variety of contributing sources. Now if you consider a whole population at any given time, by the virtue of this variety, you are going to see variations in the morphology of the population. That's where the natural selection model meets the genetic model. Of this given variety, one may possess a distinct advantage over the others. In the figure below, I combined the above two figures. Now assume that a helpful morphological mutation occurred in the yellow individual that propagated to their offspring:
Within the overall group the yellow individuals will have the advantage, therefore will have more offspring. Now suppose a calamity happens and only the yellow individuals, by the virtue of their advantage, survive. The end result will be a population that will be yellow as a rule and other variations would be the exceptions. So you need both genetically driven morphological radiation and natural selection to render the different morphologies that we see today as the result of millions of years of genetic morphological tinkering, interspecies relations and environmental conditions. Genetic, molecular, evolution would be the impetus of the morphological flow, and the environment (including all of the interacting species), would be the gatekeeper. The gatekeeper would hinder the unstable, inefficient designs and the stable, efficient ones would perpetuate. And that links up with the last section, evolutionary creation is both directed and accidental. The drive is the molecular evolutionary machinery, and the question mark is the larger environment as the whole. Think of the dinosaurs, they were doing just great for millions of years, then wham, an asteroid decided to park itself right on top of them (which is a good thing, for us, because that's how we had a chance to get here!).
Chapter Key: Morphological Flows, entities going through functional constructs thereby creating more complex entities with more complex functionalities:
DNA-(t+m)RNA-Protein functional aggregates == accretion mechanisms (Electro-Magnetism) ==> coalesced DNA-(t+m)RNA-Protein functional groups
DNA-(t+m)RNA-Protein functional aggregates == mutation mechanisms (various) ==> mutated DNA-(t+m)RNA-Protein functional groups
DNA-(t+m)RNA-Protein
functional groups + supporting material in the environment ==
constructor (accretion?) ==> functioning cell
functioning cell == replication and differentiation ==> functioning cell clusters and groups (organs)
functioning cell clusters and groups (organs) == cell-cell signaling, communication and transport ==> functioning organism
functioning organisms == natural selection + genetic accretion/mutation ==> functional speciation
And the key to successful speciation is the type of accretion/mutations that are agreeable to establishing the emergent valid (stable) state. Natural selection sees to that. Conversely, natural selection weeds out disagreeable variants that result in unstable (invalid) states.
Links:
From atoms to molecules and cells to tissues - DNA, RNA, proteins, sugars, etc. a great site
Nice article on Hox gene variation and evolution
Nice article on gene expression and limb development
Workshop proceedings: The control of size and shape in skeletal morphogenesis
Detailed work on the morphogenesis of Dictyostelium discoideum slugs
Talking Glossary of Genetic Terms