The claim by @Sy_Garte was that for any given enzyme there are a multitude of ways to make it (referring to sequences that would work). This is true for any protein, and transcription machinery is no exception.
Whatever the specific DNA changes are, there is not just one. And if you are really curious about what they are, you can read the 2014 paper on the mudskipper genome. Enjoy!
Cancer is the result of failing transcriptional regulation often due to a few delirious mutations. The story of lots of function is only true in some cases. Even where it is supported, like binding ATP, the odds of success are still as rare as 100 billion to one for a short peptide chain. (Szostak experiments) The claim you made that this is true in any protein is not supportable by experimental data and contrary to current evidence.
False. Cancer is a family of diseases caused by various types of mutation. Many have nothing at all to do with transcription.
False. Multiple review articles (not to mention the primary literature they summarize) cover flexibility in primary sequence in proteins of all sorts, and that doesnât even address the fact that multiple completely different structures can sometimes do the same job. These are basic facts of protein function that you should learn before posting more on the topic.
No idea what youâre even talking about, but that statement is hopelessly vague. And I know Szostakâs work quite well: what experiments are you referring to here?
The opposite is true. I donât know of any protein that must be 100% conserved at the aa level to maintain function. And Iâm certain you donât either.
I think it is clear that you donât understand this subject.
The metaphysical extrapolations of theology by deeply religious men speculating about the Universe is hardly unusual. Socrates is one of the most famous of those attracted attention in this way.
And each time new discoveries are made about the Universe, it can affect some of the extrapolations proffered centuries ago, generations ago, or just a few years ago.
Some religious men extrapolated from Genesis, incorrectly, that there just couldnât be anyone living round about the Southern pole of the Earth.
Some religious men probably looked for a fish or whale big enough to swallow Jonah.
Others still invest thousands of dollars to explore Asian mountain ranges, looking for remnants of the Ark.
I would ask you, who are you to say that corroborated findings about the nature of the Earth and the Universe are insufficient to justify adjustments to metaphysical extrapolations?
Even human fetuses have webbing on their fingers and toes, which usually disappears before birth. Sometimes it is retained. Some dog breeds have webbed feet. Same with some other animals. So webbing is no big deal. They donât need to develop itâthey just need to retain what they already have!
There is new information, not only from protein sequences, but also from gene regulatory networks (which is what I am working on) and further back on metabolic pathways, related to what Wagner calls âgenotype networksâ. Thanks to the robustness that is a feature of all of these systems (and all of biology), it is possible for one step changes to permeate a vast genotype space without serious loss of function. This extended network of genotypes, due to further one step events, (such as single mutations), means that not only are there a large number of multiple degenerate genotypes, but that many of these will be quite far removed (in genotype, but not in phenotype) from the original structure. Once this happens, it is fairly simple for a further single mutation to convey a new functional phenotype.
I know this is pretty cutting edge and has not been firmly established, but it is a beautiful hypothesis with some good experimental support, and I expect more will be coming.
I would echo @sfmatheson on cancer causation. Mechanisms for carcinogenesis are highly varied, and include mutations causing changes in function, as well as regulation, but these are extremely rare (or we wouldnt be here).
Can we back off the âstop posting until you understand this betterâ type admonitions? Thanks.
Yes, agreed. Sorry about that. There are better ways to make the point.
I have read Wagnerâs book and agree he has interesting ideas. It will be a real challenge to push this past the âjust soâ story phase.
They are rare because of the robustness of DNA repair. Since mutations are the core of the current theory, a repair mechanism that is remarkably robust and prevents variation must be addressed. The cell is designed to minimize variation, yet the theory requires variation. How many mutations can I have per cell division and still successfully reproduce a human requiring a trillion cell divisions?
I disagree. The basic outline of his âinteresting ideasâ is already known to be true. He has published numerous basic research papers, all cited in his book, except for the ones published since then.
Itâs been addressed. DNA repair mechanisms (and their breakdown) are well known and the subject of deep and intensive study. Studies of mutation rates (which are abundant) are de facto studies of the balance between damage and repair.
And that variation is a hard fact, subject to rigorous quantitation.
Hard to say. Why does it matter?
What does known to be true mean?
How can life exist if random mutations that escape repair are abundant? Genomes by definition will break down into non function.
Established by experimental data.
I wrote âStudies of mutation rates (which are abundant) are de facto studies of the balance between damage and repair.â The studies are abundant. Mutation rates, which reflect the balance between damage and repair, are widely studied and well known in thousands of contexts. The mutation rate is not zero, ever.
It is not zero ever but is it enough to transition species. So far there is no experimental evidence that supports a transitional event. Wagnerâs work is still theoretical. Until you can establish that the variation is high enough to support evolution you are dead in the water. So far the mutation data in the germ line is still sketchy.
Gosh, none of this is true. There is a vast literature on variation, and brand-new data on direct measurement of germline mutation rates (by sequencing direct descendants). I simply canât imagine why you write these things. Theyâre just false.
Would you be willing to explain what you mean by âso far there is no experimental evidence that supports a transitional eventâ?
Actually, as Steve said, there are some good papers that support the theory with experimental data, mostly for metabolic pathways, and to some extent for protein sequences. The evidence for regulatory circuits is so far mostly theoretical, but thatâs largely because it is a very difficult system to get experimental data from. Also, while others have published theoretical confirmation of Wagnerâs work, there does need to be wider confirmation. But I believe it is coming (hopefully, even from me).
As far as the mutation rate, it is well known, and surprisingly constant across phyla. Yes, DNA repair is extremely efficient, but it cannot be 100% because as you say, that would stop evolution. Any organism that suffered no mutations would not evolve, so there is selective pressure against a perfect repair mechanism. since such organisms could not adapt (even by micro evolution) to any stress.
Whether the very low mutation rate is sufficient to allow for the evolution we see is a good question. But we need to remember that we now know (and I refer you to Michael Dentonâs recent book, which I am sure you have read) that the single point mutations that are subject to repair are not the only mutational mechanisms responsible for innovation in evolution. Once we include transposon insertions, duplications, horizontal gene transfer, regulatory changes, epigenetic changes, etc. none of which are easily repairable, we have a very rich source of innovation for new evolutionary features.
One big mistake Creationists (and anti-Creationists) make in using probability arguments is to assume that events in sequence of events comprising some process are independent and then to multiply these probabilities together to get a very small number. That doesnât work even if the events are independentâfor example, 30 events each with a probability of 0.9 gives a probability for the sequence of (0.9)^30 = .033, a small number. It is even a worse mistake if the events are not independent, but each arises as a consequence of some physical law, Consider, for example, the properties that are life enabling (see âThe Theology of WaterâIs Design Intelligent?â. All these properties of waterâimprobable in each instanceâarise as a consequence of quantum mechanics and electromagnetic theory.
One of the key adaptive systems of mammals is the immune system but this is designed to adapt through hypermutation. The reason it works is that the binding site is limited so the search is limited. DNA repair accuracy in mammals is not yet understood as far as I know. It has been measured in single cell organisms to be about 1 error every 10^11 nucleotides during cell division. We know that error correction is also performed before transcription so we have 2 passes of correction prior to transcription. I have calculated that there would be 22 trillion mutations from zygote to adult if accuracy was 10^11. I can supply raw calculations. 22 trillion mutations seems way too high. Much higher accuracy would lead to no raw material for SNPâs we are observing when we compare mammal DNA.
It is well known, the topic of hundreds if not thousands of papers. All easy to find on PubMed.[quote=âBillcole, post:79, topic:35420â]
I have calculated that there would be 22 trillion mutations from zygote to adult if accuracy was 10^11. I can supply raw calculations.
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Please do. I suspect an error or two.
Do your calculations account for apoptosis induced by unrepaired DNA damage?
Or for the fact that the germline is set aside quite early in development in mammals?
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