Questions about recurring mutations and phenotypic convergence

[QuarkHead]

And by the way Maddad, and others. There are some very knowledgeable and helplful people on this forum who, if asked a genuine question, will be only too happy to oblige. Everybody likes to parade their genuine knowledge! But if you come on telling people they are "wrong" when they're not, it can be a very unforgiving place.

 

[Hercules Rockefeller]

And by the way Maddad, and others. There are some very knowledgeable and helplful people on this forum who, if asked a genuine question, will be only too happy to oblige. Everybody likes to parade their genuine knowledge! But if you come on telling people they are "wrong" when they're not, it can be a very unforgiving place.

And who, exactly, are these "others"? I hope you're not referring to me. I told Maddad he was wrong because he is. He clearly doesn't understand what he is taking about, and you agreed with me.<P>

 

[QuarkHead]

And who, exactly, are these "others"? I hope you're not referring to me. I told Maddad he was wrong because he is. He clearly doesn't understand what he is taking about, and you agreed with me.<P>

Hey Herc!! You most definitely ain't one of the "others". You are one of the K & H (decode!) I referred to.
But don't go away. I've got something I want to try out on you

 

[QuarkHead]

And who, exactly, are these "others"? I hope you're not referring to me. I told Maddad he was wrong because he is. He clearly doesn't understand what he is taking about, and you agreed with me.<P>

I've kept in this now irrelevent header so you know this post is directed (principally, but not exclusively) to you.

Accepting the standard evolutionary paradigm, let's agree on two facts. Complex organisms have more DNA that simpler ones, and they also have more genes (that, I assume is what makes them more complex) Let's say there is corresponence between these two facts.

The only known way for a genome to increase in size is via amplification, right? So what this seems to imply is that, at some stage in the evolutionary process, there will have existed an intermediate form with n-tuple copies of each gene. Let's call them gene families. Oh and by the way, let's also agree that the progenitor form was quite well able to carry out the functions necessary for life on Earth with only one (at most two) copies of each gene.
What you seem to have, at some stage of evolution, is an intermediate form with (n -1)-tuple copies of each gene, surplus to requirements, so to say.

Now these "extra" genes are free to do whatever they please, usually without detriment to their carrier. They can, if you like, be "experimented" on by the evolutionary process via mutation of any sort you care to imagine.

Let me say, as an aside, that the gene families we already know of have a far greater repetoire of mutational possibibilities than do singletons.

So what you would then have is an evolving organism, free to try out any new form of a gene that was orignally for an essential function without any detriment to itself. Obviously, if the new gene were a distinct advantage, then it would be selected for and remain fixed in the population.

Looking at it this way, you might account for a number of things. First, fixation of neutral alleles. The problem for a population geneticist doesn't go away, but it is put in a different perspective.
Second it might go some way to explaining punctuated equilibria i.e. the absence from the fossil (or any other) record of intermediate phenotypes.

I could go on but I can see you're nodding off......

 

[Hercules Rockefeller]

Apologies to Danniel for subverting your thread! <img src="http://www.fadzter.com/smilies/bubbly.gif">

I could go on but I can see you're nodding off......

No, I was just resting my eyes. <img src="http://www.fadzter.com/smilies/sleep.gif">

The mechanisms of evolution are not my strong suit, but I don’t have a problem with anything you’ve said. To my reasonably limited knowledge of the subject you have, in a general sense, summed up the process of the creation of gene families fairly well, although I’m not sure I immediately concur with your punctuated equilibrium speculation. I’d have to think about that some more.

Conservation of gene duplicates can occur when one gene acquires a new function ("neofunctionalization"), or when the ancestral function is divided between the two duplicates ("subfunctionalization"). As it happens, I was just reading a perfect example of subfunctionalization. In zebrafish embryos, <I>hoxB5a</I> and <I>hoxB5b</I> are expressed in distinct domains, and their combined expression domain is equivalent to that of single <I>Hoxb5</I> genes in other species (<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11440248" target="new">Bruce et al., <I>Evol. Dev.</I> 3 , 127-144</a>). <P>

 

[Maddad]

Replication has nothing to do with coding for proteins, "right" or "wrong" ones. Replication merely copies DNA. The code as you so quaintly call it is broken only by the translation machinery...and only that.

Replication has everything to do with coding proteins. If you code the DNA or RNA incorrectly, then the miswritten code will then try to make the wrong protein. Since the celluar machinery required to support the next generation depends on those proteins, it won't happen and replication stops.

You can't get away from it Quark. If you don't code correctly, everything goes to hell in a handbasket and stops.

Please compute for us the probability of generating a transcrition or translation stop signal from any arbitrary pair of codons after a frame shift.

That's easy. Most biological processes recognize three base pair combinations as stop signals. Since there are 64 (4<Sup>3</Sup>) possible combinations, and three of them are stops, the probability is 3/64 or about 5%.

 

[QuarkHead]

Replication has everything to do with coding proteins. If you code the DNA or RNA incorrectly, then the miswritten code will then try to make the wrong protein.

This of course is true, although the error rate in replication is extrememly low, due to the presence of an editing machinery

....it won't happen and replication stops.

But it doesn't stop, any more than a photocopier wouldi f your documant has a spelling mistake

That's easy. Most biological processes recognize three base pair combinations as stop signals. Since there are 64 (4<Sup>3</Sup>) possible combinations, and three of them are stops, the probability is 3/64 or about 5%.

What you say is partly true (although it is customary to normalise probabilities). I know of no life forms which will use any one of the 3 known stops with equal facility. No matter. But what does matter is you have answered the wrong question i.e. you have computed to probability of getting one of 3 possible stops from coding triplets by point mutation.
That was not the question, It was you who first asserted that frame-shifts always generate a stop. Why I couldn't be arsed to do it myself is you need a table of all the coding triplets, arrange them in all possible pairwise combinations, and see how often you get a stop by shifting the reading frame by 1, 2, 3....n bases to the left. It ain't trivial.
No marks for answering the wrong question!!

Edit: I should, of course, have said shifting to the right

 

[Buckaroo Banzai]

I can only geuss at what you are saying here. Let me say first, though, I know almost nothing about development in general. But - I do know that it is a popular fallacy that because something is there, then it must have been selected for. Example - look in the mirror, there, right beneath your nose, do you see a double fold? (maybe you have a beard!!). That fold is not "selected for", it is just a consequence of the way the embryo develops.
I would imagine (again - I'm no expert here) that tails are the default design for all vertebrates, and they are only "discarded" in the evolutionary sense when they either become a nuisance or can easily be dispensed with.

Well, I agree with all you're saying... my point was just that tails will more likely remain genetically recognizable as homologous rather than look that arised independently by the accumulation of lots of mutations that do the same thing as the "original" tail genes do. Even if the tail development were nearly completely genetically independent of the rest of the vertebrate development (which isn't), and somehow (magically) mutations that affect tails were completely neutral to the rest of the body, tails would yet remain with the most of the same genes...

Ahhh! I'm starting to get suspicious here. Why do you want to trace wrong phylogenies? Have you a better one than the standard? Does it matter?
In one sense, no it doesn't - phylogenies are merely our way of collecting stamps and keeping the natural world in our sort of order. On the other hand, if you choose to re-classify our existing phyla and their relationships, say "all things with tails or flagella in this box, all things with light receptors in that one" then you would have a very very very hard time coming up with an evolutionary model.

It was all related to an anti ID creationist argument. They use to allege that the genetic simirities are due to phenotypic/functional similarities. I've used to answer that if that were true, phenotypic convergences could have in many instances the same genes behind, which doesn't happen at least in long-distance. For example, plant-mimetic insects (if we could call it a convergence, but doesn't matter in this situation) have no more genes in common with plants than the non-mimetics, nor chlorophyl or chloroplasts; but I'm not so sure with "convergences" with closer ancestry; species in which a structure is retained from a common ancestor certainly have lots of the same genes involved in the development of this shared structure; subtle changes in this structure can also be genetically similar if there are shared silent genes, which could be activated by different mutations in different genes.

That would make it look a lot like as the structures were intelligently placed in two different organisms, because the only genetic difference would be in the regulator gene, not in the genes that directly influence the development of the structure. So would be technically possible, I think, to get wrong phylogenies if only these specific sequences were analysed in certain species.
But I think that it should be pretty rare, and if a IDC were going to gather tendencioulsy selected data to prove something like that, it would be a evident fraud... but yet convincing to someones...

 

[QuarkHead]

Well, I agree with all you're saying... my point was just that tails will more likely remain genetically recognizable as homologous rather than look that arised independently by the accumulation of lots of mutations that do the same thing as the "original" tail genes do.

Well, be careful here. There is definitely such a thing as phenotypic homogeneity on a genetically heterogenoeus background. Which is just a grand way of saying "convergence" except, if I put it like that, I don't imply selection.

Ooops. I deleted your next bit. But I think this is relevent. Remember that the genes that control devolpment (mainly hox) are about the most highly conserved that we know of. Structures that we think are intrinsic to development (I was trying to say that tails, for example might be) will probably always occur in the vertebrate (chordate even??) lineage, unless there is a pretty good reson not to have them. My point being....you dont need to select for a tail because it's there by default. But you may be able to select against it's expression. But even there I bet you would always be left with an anatomically recogniseable vestige (like our coccyx)

They use to allege that the genetic simirities are due to phenotypic/functional similarities.

Well go back and remind them that genes determine phenotype, not the other way round. Yep - you were right and they were wrong! (did you ever doubt it?) Creationism. HA!!!