The evolution of the protein coding genes

[mark kennedy]

Presumably the vast majority of frameshifting indels will be immediatly lethal and get removed from the genome, often before even going full term. This will leave only the non frameshifting indels, the ones that are a multiple of three base pairs, to play any role.

How does the lethality of the +1 or +2 have any bearing on the effects of non frameshift indels?

Out of a hundred how many indels do you think can happen in a protein coding gene and not result in a frameshift. The fact is that most of them are probably not lethal but the vast majority of those having an affect will be eliminated by natural selection.

Contrary to the common assumptions of Darwinism mutations simply do not result in viable adaptive evolution most of the time. Most adaptations are the result of recombinations of intact genes.

You are also missing the most important point in all of this. This is nothing more then a comparison, only the differences are thought to be the result of mutations. It's simply not possible for random mutations to pull something like this off and scientists, if they are being honest know this. As a matter of fact they readily admit to this in their peer reviewed publications.

 

[Assyrian]

Out of a hundred how many indels do you think can happen in a protein coding gene and not result in a frameshift.

33?

The fact is that most of them are probably not lethal but the vast majority of those having an affect will be eliminated by natural selection.

In a small population, unless they are lethal, significant numbers of neutral, beneficial and the less harmful mutations will be fixed in the genome simply through genetic drift.

Contrary to the common assumptions of Darwinism mutations simply do not result in viable adaptive evolution most of the time. Most adaptations are the result of recombinations of intact genes.

What is an intact gene? One we share unchanged with yeast?

Or do you mean adaptation does not usually wait for a new mutation to come alone, but involves recombination of the entire gene pool, including mutations that occurred long before?

You are also missing the most important point in all of this. This is nothing more then a comparison, only the differences are thought to be the result of mutations. It's simply not possible for random mutations to pull something like this off ...

Why not? We have already seen how the difference in point mutations between the genome fit the rate of mutations that occur per generation. Why should indels be any different? The lethality of the 67% frameshifting indels tells us nothing of the other 33%.

and scientists, if they are being honest know this. As a matter of fact they readily admit to this in their peer reviewed publications.

You will find scientists questioning the precise mechanisms going on in many areas of science. It is the way research works. How many of these actually think their questions will lead to a scientific revolution and overthrow of the conventional theory, and how many simply see it leading to a better understanding of one small area?

But this is just falling back to general questions that have been gone over again and again. I still do not understand why you bring up the lethality of the frameshift indels when it says nothing about the viability of non frameshift ones.

 

[Xaero]

Hello Mark,

Your missing the most important issue here, whether it's a loss or gain the results of indels are most often either neutral, harmful or even deadly.

Where's the problem?
Lethal mutations cannot survive -> will not get inherited: Next (mutated) candidate please...
Mutations in important coding regions are sometimes already lethal at the embryonal stage.

I guess we will get into this later because there should be an explanation for the elevated mutation rate.

*sigh* this is the message i wanted to get in your head: Because the CpG sites are methylated!
In detail the cytosine that is methylated desaminates into thymin instead of uracil - this mutation is harder to detect by repair mechanisms -> resulting in higher mutation rate. There is also a higher rate when there is more GC around that region: http://mbe.oxfordjournals.org/cgi/content/full/22/3/650
God even created Methyl-transferases to catalyze the methylation of DNA for different purposes. There are also hotspots of recombination with an overabundance of CpG.

btw, the ability of nylon-eating that arrived in Flavobacterium seems like a gene duplication with a frameshift mutation.
I was looking for such a mutation - here we have a gain of information and a beneficial frameshift

When i read through technical literature on the open peer-reviewed online magazine PLoS i see lots of mechanisms explaining higher mutation rates, so it seems like the Creator did create these mechanisms for a certain purpose. Just search for recombination, mutation ,hot spots, micro satellites.

I don't want to insult you, but to me it seems like your attempt to point to genetical problems are nothing more than punches into air (or you are simply outdated).
I wonder if your fellow creationists are understanding one bit of what you are saying.

So far,

Xaero

 

[shernren]

A point mutation can cause a frameshift, just imagine what a major change can cause.

gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins) Nature 2004

What you're not getting is that even a single base indel's frameshift is a major change by the metric used in that paper.

The ironic thing here is that the PTR22 is the Chimpanzee Genome. It is the human line that underwent a major change, not the chimpanzee.

How would one determine this without access to the ancestral genome of both?

 

[Xaero]

How would one determine this without access to the ancestral genome of both?

http://genetics.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pgen.0020168

Comparative genomics allow us to search the human genome for segments that were extensively changed in the last ~5 million years since divergence from our common ancestor with chimpanzee, but are highly conserved in other species and thus are likely to be functional. We found 202 genomic elements that are highly conserved in vertebrates but show evidence of significantly accelerated substitution rates in human. These are mostly in non-coding DNA, often near genes associated with transcription and DNA binding. Resequencing confirmed that the five most accelerated elements are dramatically changed in human but not in other primates, with seven times more substitutions in human than in chimp.

 

[shernren]

Ahh. I missed that. Thanks.