Sunday, February 24, 2008

Evolution - The scientific method

I believe strongly in the development of evolutionary science, and I have new hypotheses that ought to be tested that don't contradict any experiments done, nor do they contradict the overall modern evolutionary synthesis. However, these hypotheses, if proven, may open up some arguments thought long ago settled.

The role of random mutations is well researched. These are well observed and are thought to be the basic unit of truly new, potentially beneficial adaptations.

DNA repair 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.

In this sense, this hypothesis is not concerned with the genetic variability due to the shuffling of phenotypes that follow the laws of Mendelian Inheritance, 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.

Tuesday, February 19, 2008

More Rants

There are clearly other biological hypotheses that have somehow graduated to the orthodoxy, such as Earthly abiogenesis. The hypothesis that non-life to life transition happened on Earth is a reasonably testable one, but a lot more mileage is given to experiments that assume early Earth origins (ie. that somehow Earthly origin is almost certainly the "truth"). However, I will concentrate on those biases against anything that remotely appears Lamarckian or like intelligent design (even if the intelligence is held within the DNA and/or the organism itself).

Now my thesis is that although the main feedback of information back to the DNA of how well it is doing is via the brute force of "natural selection" - that is a comparative between individuals with different DNA. However, my thesis is that there clearly is processes that are very much like selection that is also giving a feedback of how "fit" the DNA is. There are tens to hundreds of millions of sperm that are competing for an egg. The male is producing these and there may be a selection process from that side which strengthens those sperm with particular mutations and weakens others depending in part on the level and type of stress he is under. 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 ova. The ova 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.

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 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.

The difference between the orthodox view and my view can be illustrated by a fashion paradigm. In the orthodox view, fashion designers make random changes to existing designs and force models to wear them. If they sell, they make more of the same. If they don't, the clothes get thrown in the bin and they don't make anymore of that crap.

In my view, what (successful) fashion designers do is that fashion designers make random changes to existing designs - show them to a test audience (of horny males, apparently :)) - changes that show some approval get kept. Process is repeated as many times as the exhausted sewing machinists and test models can cope with and then the surviving clothing is forced onto the model and onto the catwalk.

In my more sophisticated fashion design view, the machinists and models are given a break and all the experimentation with random changes happen on the computer (or a drawing board) and get shown to the test audience. By the time the design gets on the catwalk, the design looks "worked" and unlike the designs it may have been based on. To an untrained eye, it might still look like random changes, but those that *actually* put random changes straight on to the catwalk don't win the fashion show.

Additionally - to look at it another way the *winner* of the fashion show can gloat and make grandiose claims about his *creativity*, when in truth he just had a more sophisticated system of randomised changes with good feedback loop.

Monday, February 18, 2008


My research on modern ideas on Lamarckism has led me to Edward Steele, a controversial Australian Molecular immunologist. He has (indirectly) demonstrated a counterexample contradicting the Weismann Barrier. Now my instinct (as was his) was to suggest that the Weismann Barrier is therefore disproven, and we should be looking more closely as to when, why (or why not) there would be information feedback from somatic cells to germline cells.

I would also suggest that the Central Dogma of molecular biology should not be taken as gospel in evolution. It is not a proven fact as such - it is a simplification that demonstrates the orderly passage of genetic replicative information. It says nothing at all about the exceptions to this process (mutations). However, it is the very exceptions to the process which drives evolutionary progress. Natural selection is the big feedback loop for information about the environment to (indirectly) affect DNA. I am certain that there is extensive natural selection between sperm - However, this isn't exactly comparing one's fitness with others, because they are all from the one organism. An elaborate error correction mechanism (to obtain the best possible duplication of genes) is not actually selecting at all. It must be practically a simulation of how fit they will be in the environment - letting through genes and mutations that "pass the test" which must be indicative enough of adequate fitness through a living body.

Saturday, February 16, 2008

Dillemma - Conviction Rant or Scientific Method

I am not sure whether to use this blog to state what I believe the scientific truth to be, or whether to methodically and scientifically (with citations) demonstrate why I am right.

At this link - The crux of the matter is laid out a plausible genetic mechanism for "smart" mutations that would clearly be a superior response to stresses than "random" mutations. If that kind of response is actually possible in an organism, those organisms that express this response would clearly be "fitter" than those that don't. In a purely Darwininan way, those without capability for "smart" mutations would not exist anymore.

Thursday, February 07, 2008

Selective stress-breeding to create a long-neck

Background: This system presumes that my theory is completely correct (I do). Artificial selection is all well and good and has a proven record of succeeding in breeding stock with desired characteristics. However, the characteristic in question must exist in the population to start with. This is highly unsatisfactory and there is just no way you could, say, breed an antelope with a considerably longer neck (or taller all round, like a giraffe) without triggering appropriate mutations first.

The trick would be to find the same stress/mutation trigger that caused (say for the giraffe) those mutations required to be more prevalent, which allowed natural selection to have something useful to select from and speciate a taller (long-neck) animal.

The first condition is to pick an animal that feeds on leaves. There is not much point picking a carnivore or a herbivore that only eats grass/fruit etc. because there is no natural situation in geologic history in which a long neck would be the difference between life and death for such. I choose the antelope in this case - it eats leaves and lives in the same continent, so might share the required triggers and responsive genetics.

The second condition is that the breeding stock must be in some kind of stress. This is considered animal cruelty, so I suggest any experiments are done in a subsaharan country that is in a state of war: Nobody notices any cruelty that happens in those countries. Stress is well known to trigger mutations and is highly necessary to accelerate the process of artificial selection.

The third condition is to pick a stressful situation appropriately. Adaptive mutations happen as a mutation response that succeeded in the geologic past. They may not be apparent in the animal because they eventually reversed in the normal cycle of things - hopefully numerous times in the species' history such that it reinforces the response(s). In the case of the antelope, the stressful situation might have these features:
1) Near-starvation. This is known to also have physiological responses of delaying maturity, among other things. It is likely to trigger responses that might achieve it more food for its progeny in analogous situation.

2) Declining and/or isolated population. This reinforces that it is likely to be a long term stress, and which migration is unlikely to resolve. Inbreeding and polygamy might be physiological indicators of this.

3) Visual cues that food is plentiful higher up. Perhaps just out of reach, or even selective cues like seeing that taller relatives are better fed.

4) A lack of predators. Predators are known to put selective pressure towards earlier maturity thus smaller form.

I don't know if penning up antelopes, while at the same time putting heaps of food just out of reach of all but the tallest is an ethical way to prove Lamarck right - But I think that is exactly the sort of thing that led to Giraffe's long necks, and could be demonstrated within the space of a few lifetimes.

Tuesday, February 05, 2008

2nd draft "Marconomic Theory of Regressive Evolution"

Mainly for clarification, disambiguation and to match experimental evidence?

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).