Please feel free to comment and participate on theknol link of this subject. Real research can elucidate on this subject and a knol is an ideal way to bring together ideas.
On the origin of mutations leading to speciation, adaptation and evolution under changing environments, stresses and niches. Natural selection is viewed as the catch-all backstop of adaptation, while guesses based on detailed meta-information garnered over millenia of generations filter mutations to a useful subset of completely statistically random mutations.
My theory, is concerned with "Macro mutations" and in its plainest form just expands on what is already known. I will use the term DNA subroutine for a gene that can be switched on or off to express the macro mutation in question.
Fact: an organism under stress exhibits considerably higher mutation rates.
Theory: Different types of stresses will confer different spectrum of mutation - ie. the mutations will favour more likely beneficial mutations for a predicted future requirement which the stress would signal.
The mechanism proposed is that over a window of genetic experience (say a million years) the DNA stores information regarding which mutations were more appropriate for the given stress and which ones weren't. A "bank" of hundreds of thousands of DNA subroutines that has built up over time and proved their worth are either expressed or switched off to save metabolic resources. If a subroutine has been switched off long enough it can be relegated to "junk DNA" status and will not further be trusted in the field due to it being no longer valid in the new context (or from an orthodox perspective become unusable due to genetic drift)
A word on micro mutations:
Micro mutations are classified as completely random errors in duplication of genes. These are strongly evident and well studied. However, the orthodox view is that the only way for these micro mutations to avoid eventually destroying the function of the gene in question is for them to be field tested by natural selection. To put it another way, the whole organism has to die before reproducing to avoid one crucial micro mutation from being copied. I find this argument incomprehensible. It is like as if the only way to avoid errors in programming the oxygen intake valve of the space shuttle is to launch it anyway, let it crash and avoid using those blueprints again. I call it the crash, burn and learn concept. It might be alright for a virus with millions of launches every second, but I don't think it would quite be so good for the Emperor Penguin.
This lends itself to my belief that there is something else at play other than natural selection. There must be some sort of error correction or testing mechanism on individual DNA subroutines, and if there is, they can just as easily apply to non-expressed genes (or, much more likely, there is a system that expresses these, but localises them for testing only, thus suppressing the evolved purpose of the DNA subroutine for that generation at least).
Repair - see - DNA">http://en.wikipedia.org/wiki/Dna_repair#DNA_repair_and_evolution">DNA , Is a process where damage to the DNA is fixed. This process is imperfect, however and failure in repairing mutations is a variable source of mutations. The process of DNA repair is blind to the function of the gene it is repairing. Thus, resulting mutations tend be in random places, and the build up of mutations on sections of DNA that don't change the function of the gene happen at a well defined rate. Thus, a process of feedback of information whether the gene is functioning properly, is the only way to account for genetic drift NOT occuring on important functional elements of the gene. Natural selection acting on whole organisms holding that gene is the only feedback commonly agreed on by evolutionary biologists to occur. However, my view is, that with a hierarchy of genes (ie. genes that control a bank of genes, that each control a set of basic genes that relate to a phenotype), there needs to be a hierarchy of feedback to ensure that the lower level genes are functioning. Ie. there needs to be a form of selection within an organism such that each basic gene can be selected or rejected based on its function independently of all other genes. The corollary being that lower level genes that are suppressed in some way by some higher level genetic action, can have its function ensured with the same process of feedback.
There are a number of mechanisms that could be at play to ensure functional integrity of genes, that are not natural selection between whole organisms. One of the mechanisms proposed, which is quite likely to be involved in some way is through the selective properties of sperm. In this mechanism, sperm act as selective proxies for the organism but specifically for genes lower down in the genetic hierarchy. Thus, every lower level gene affects the selective aspects of sperm, and that which gets to reproduce has fully functioning lower level genetics.
On the female side, the same thing is bound to be happening, with body conditions slowing down sperm with some particular mutations and letting through others depending on the level and type of stress she is under. As a final error correcting check, particular important sequences of genes are tested in the controlled conditions of the ovum. The ovum has been fully formed since before the mother-to-be was born. This is a rudimentary "archive" that checks on crucial DNA sequences to make sure there is no changes to those. Thus, a great deal of crucial environmental and/or competitive information is fed back to the DNA, as well as strict error correction on crucial segments during and even before conception. Thus the new organism will have had extensive pre-birth selection to give its genes the best chance of survival.
In this sense, this hypothesis is not concerned with the genetic variability due to the shuffling of phenotypes that follow the laws of Inheritance see - Mendelian">http://en.wikipedia.org/wiki/Mendelian_genetics">Mendelian , but only the functionality of the individual allele itself. This hypothesis takes it as a given that the spread of mendelian traits is the primary source of variability in phenotypes that are subject to selection in a standard Darwinian way. This hypothesis is concerned with:
1)How "improved" versions of alleles arise.
2) How stress triggers greater mutations.
3) How latent phenotypes not visible in a species can become common again.
4) How many "truly new" genes are involved in speciation, and how many genes are latent ones that are re-activated (or de-activated), or inserted via horizontal gene transfer, or are just a previously unobserved combination of mendelian and non-mendelian traits.
This might yet be uncontroversial - But it really depends on how sophisticated the stress to mutation-selection link is. To me it is plausible that there is a simulation engine powered by the subconscious mind that does intense calculations on how well any particular mutations may benefit particular constraints. Information can flow through the sub-conscious mind, seeing certain genetic consequences, and the subconscious could translate it to stress information that would be selective for sperm proxies of the same genetic consequences. These would be really, really smart mutations - Much smarter than any genetic engineer could ever hope to become in following millenia.
