Re: [asa] Anybody familiar with Sanford's book?

An excellent response David. Thanks for taking your time to address
these issues from a scientific perspective.

On Dec 18, 2007 3:50 PM, David Campbell <pleuronaia@gmail.com> wrote:
> "near-neutral (very slightly negative)"
>
> Near-neutral are about as likely to be slightly positive as slightly
> negative, though "natural selection acts on the entire genome as a
> whole, not individual nucleotides" is in fact a major problem for
> labeling near-neutral, or even many more dramatic mutations, as
> positive or negative-we can easily tell, e.g., that a mutation makes
> an enzyme a bit more or less efficient, but determining the overall
> effect on the well-being of the organism (if any) is much more
> problematic-too efficient an enzyme could throw other things out of
> balance. The other major problem with various antievolutionary claims
> that mutations are usually negative is that negative or positive is
> almost entirely situation-dependent. Something that always kills you
> before you can reproduce is guarenteed not to be beneficial, but it
> also eliminates itself form the populaiton automatically. However,
> sickle-cell anemia, near lethal in homozygotes, provides significant
> resistance to malaria in the heterozygote-a seemingly bad gene
> actually turns out to benefit in the particular set of pressures.
> Mutations that are strongly positive or negative have correspondingly
> much higher probabilities of spread or elimination in a population.
> Not only does the environment vary, but there are different possible
> scenarios within an organism. If a gene is just beginning to take on
> a new function or a genome is encountering novel conditions, the
> probability of a mutation generating significant improvements is
> relatively high, as is the probability that the organism can get by
> with a poorly functioning version. If a gene has long functioned in
> its present role, it's probably fairly well refined and subject to
> only minor improvement, and it may be relatively imortant to an
> organism.
>
> "rarely can negative mutations be separated from positive ones"
>
> Misleading. ALL negative mutations are difficult to separate from ALL
> positive mutations, but any given mutation sorts independently of any
> other unless it is fairly close to another on the same chromosome.
> Thus, in most cases it's fairly easy to separate them. There are
> examples of such linkages, however. For example, strong jaws and bad
> backs are associated in the dog/bear group of carnivores, specifically
> in pandas and bulldogs.
>
> > Since it has been demonstrated that more negative mutations occur than 'positive' ones (within our lifetimes; disease, etc)<
>
> I don't know of any such thing actually being demonstrated, though
> it's popularly asserted in attacks on evolution.
>
>
> > Because near-neutral mutations cannot be selected against...they will build up
> > and their additive affects will eventually condemn the genome to extinction.
>
> No, because if the additive effects are significant (of which there is
> no guarentee), selection against the net result will become higher.
>
> > This is an inescapable fact just like if you kept introducing typos into a
> > book – the book will be understandable for a long time but eventually it
> > will lose sufficient meaning to convey the message (extinction).
>
> However, A) natural selection works to correct typos and B) numerous
> different books are all viable options. The result won't be perfect
> copies of the original, but if the copies were all perfect there
> wouldn't be any evolution.
>
> > No mutation can claim to be truly neutral, as it takes up space in the
> > genome – spacing itself (e.g. between regulating elements and their genes)
> > is important.
>
> Well, in theory any given mutation puts an organism one step closer to
> evolving certain functions and one step further from evolving certain
> functions. Similarly, there are factors that can favor a more
> G/C-rich versus A/T rich genome. If the potential for future
> evolution is discounted as a factor, however, there are plenty of
> mutations that have absolutely no effect on the organism. For
> example, although spacing is of some importance, the exact length of a
> space is not, nor the exact sequence of bases. Likewise, hundreds of
> bird species have mitochondria that do exactly the same thing but with
> slightly different gene sequences; similar patterns are seen in all
> types of organisms but that's one of the largest single data sets.
>
> > high mutation rate per individual (up to 100-300 per person per gen), there is no way enough 'negative-mutant' individuals can be removed/out-competed from the population <
>
> In reality the vast majority of these mutations rapidly disappear from
> the population (at least as direct decendants; they may reappear as
> new mutations in other individuals) due to genetic drift. Especially
> at the beginning, a mutation is present in such low numbers that it
> has a very high chance of not being passed on. For example, at the
> moment any new mutation of mine has a 50% chance of being carried by
> Timothy. If he has children, any one of them has a 25% chance of
> having my mutation, etc. Someone with significant negative mutations
> would have to reproduce a lot to make much difference.
>
> >Sanford argues that whilst there may be short term 'benefits' in some
> mutations...these are only ever losses of already existing information
> (turning-off of a gene, etc).<
>
> No, they are also production of new information.
>
> > However, firstly, wherever the free copy is inserted it will instantly
> > affect something else (reduce information) in the genome by simple
> > positioning (even if quite small effect – it will never have zero effect).
>
> Affecting something else is not reducing information, it's increasing
> it. However, there's no guarentee that there will be a significant
> effect on anything else. In particular, major methods of gene
> duplication tend to generate either copies adjacent to each other or
> copies of the entire genome (with things positioned as they were).
> Duplication associated with transposable elements is the main
> exception.
>
> > Secondly, the amount of that gene product would be instantly increased (the
> > free copy would also have to be 'on' in order to be selected for an
> > alternative function) leading to an imbalance in gene product and therefore
> > function; this could have a profound impact on other genes and/or pathways –
> > it will very unlikely have no impact.
>
> Depends on A) what signaling codes are associated with the "new" copy
> and B) what function the gene has. A recent study on human digestive
> enzymes found one that had been copied several times, improving our
> ability to digest certain foods.
>
> > Thirdly, which copy is to become the 'back-up'? Any recombination-exchange
> > between the two copies over time will likely contaminate each other with
> > their own mutations – actually quickening decay.
>
> It depends greatly on the details of function. Most likely, the basic
> structure of both gene products will be similar and the same region
> will be functional. As a result, exchanges between most parts of the
> gene will have little effect on either, whereas exchange of the
> functional regions would merely swap which gene was doing what. Only
> recombination that disrupted the functional regions would be a
> problem. However, recombination disrupting the functional region
> would become much less likely as the functional regions diverged,
> whereas if the functional regions were not very divergent,
> recombination within them would be likely not to have much effect.
> Note also some recent studies observing evidence of such processes.
> It's especially easy if the original protein had dual function-each
> copy can specialize on one of the original functions.
>
> > Fourthly, genetic drift of the free copy could easily lead to a dominant
> > negative affect on the 'back-up' (i.e. the new 'free' version will interfere
> > with the originals' function).
>
> ? Not quite sure what is being claimed here. I think what's
> envisioned is the divergent copy becoming a dysfunctional allele of
> the old version. If so, it's simply a repeat of the recombination
> point made above.
>
> > Fifthly, how would the first several mutations in the free copy be selected
> > for – this is irreducible complexity at the most fundamental level –
> > nucleotides function within the context of the surrounding nucleotides,
> > which obviously are in place for their original function – not anything new
> > (makes it more likely to become a dominant negative mutant).
>
> As the original was functional, no mutations are necessary to give
> function to the copy. Starting with a functional original, there's a
> good chance that a modification of it will give something with
> slightly different function. The idea that several coordinated
> mutations must take place is incorrect. However, because there is the
> original, the "free" copy is free to become non-functional in the
> process of developing a new function. This is also addressed by the
> possibility that the original was multifunctional (or at least covered
> both functions, perhaps by doing one generic action).
>
> > Sanford makes a nice point in the book about probability and mega-mutations.
> > I think it's Dawkins who coined the phrase 'Mount Improbable' for the theory
> > of evolution. If one is climbing such a mountain, and is prone to 'tripping
> > over' (mutation) occasionally it seems logical that you'd rarely trip-up the
> > mountain very far. On the other hand, tripping in a downward direction seems
> > more likely, and it's possible to fall a great deal further!
>
> Entirely dependent on where one is on the mountain, as well as what
> are included under "mega-mutations". For that matter, a landscape is
> much better as a picture of evolution than a mountain-from some
> places, one can only fall down; from others, up is more likely. Add
> the caveat that the landscape is constantly shifting (rapidly in some
> places, slowly in others).
>
> > One of the implications of the general deterioration of the genome is that
> > life spans could quite easily have been in the 100s as per Genesis.
>
> Reproductive output per lifespan, rather than longevity per se, is
> what would actually be selected for. There's no reason to assume that
> "better" genes would produce greater longevity (cf. Gulliver on the
> ambiguous benefits of immortality). Some genes do promote greater
> longevity, and some clams can surpass 400 years in age (the current
> animal record holder), but there's no particular reason to think that
> such is biologically "better".
>
> --
> Dr. David Campbell
> 425 Scientific Collections
> University of Alabama
> "I think of my happy condition, surrounded by acres of clams"
>
>
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Received on Wed Dec 19 13:23:02 2007