Ok, so this is more a matter of a layman wanting to ask a couple specific questions to biochemistry experts that anything else, but it might also be an interesting topic:
One of the big hurdles that creationists and other evolution-doubters have to take, is realizing that "life" is far removed from the Perfect Fragile Machine that they imagine. A random mutation really does not necessarily stop life in its tracks, there is room between "functional" and "non-functional", different roads lead to Rome on several levels... Life is robust precisely because it is not carefully engineered to work perfectly and optimally. Better to be "good enough" and have backup-strategies to remain "good enough" most of the time, than to work towards something that is perfect, but only under precise circumstances.
It might be interesting to compile a list of processes, structures etc. that illustrate this redundancy and tolerance.
In a post with a very high-level explanation on an Islam forum, I came up with this (incomplete) list. This thread would be meant to either
work out the examples I mentioned, or
correct the mistakes/oversimplifications(likely
), and to
introduce more examples.
-
junk DNA catches most mutations (not really completely on-topic in this list)
- cells have a number of
verification and
repair mechanisms which catch lots of detrimental errors
- there are more possible codons (64) than aminoacids(20), which means that there are
multiple versions of codons that still result in the same aminoacids. A mutation which turns one version of such codon in another such one, has no implications (silent mutation)
-
gene duplication errors create redundant copies of genes. Those copies can take over if the original one is no longer functional due to a bad mutation (is it a given that multiple copies will ALWAYS only have positive effect?), and they are also a laboratory to create novel genes
- sexually reproducing organisms have a "
heterozygote advantage" because they have all chromosomes/genes duplicate (except X/Y of course). One copy can be dysfunctional without fatal consequences (is it categorically NO effect if one is dysfunctional, or is there a whole spectrum from NO consequence to "not deadly but still seriously affected"?)
- an example like vitamin C illustrates that often it is
possible to take in certain essential substances (like, via food) instead of letting the DNA synthesize them internally. This is why humans and apes (and bats) have a defective gene for vitamin C synthesis without being affected. (is this a fairly unique (known) example, or is this abundant?)
- a mutation in a gene doesn't have to mean that something simply doesn't work anymore altogether; it could also mean that a biochemical reaction further down the chain will
merely execute less efficiently, while possibly they produced an excess of some essential substance already so it would have NO effect at all?
- many genes or groups of genes code for traits that
aren't essential anyway (eye color, anyone?)
And then one that I was using in a translation of the
"Cytochrome C" example in Douglas Theobald's "29", and I'd like to know how precise this formulation is:
- biochemistry with complex biochemical molecules like proteins is far more insensitive to changes in the components than the simple inorganic reactions we learn about in highschool. That is,
the reactions depend mostly on the shape of the proteins, and on the aminoacids on the "outside". And very often both of these will not be affected much by replacing aminoacids "on the other side of the chain" (for example, they could be locked up inside once the protein has curled up). Is this a fairly accurate general statement? I've read elsewhere that a small change in aminoacid sequence CAN severely destroy the structure of the curled-up protein, but would this be in a minority of cases, or is it that despite this would be the case in the vast majority of cases, there's still an astronomical amount of possibilities to have a mutation NOT influence the structure?