Yes, but the mutations almost certainly happened long before the lizards were moved to the new island.
I’m not denying that mutations occur, I’m just pointing out the false notion that evolution isn’t acting on an existing reservoir of genetic variation, that evolution isn’t happening without new mutations.
That’s Tom’s and Marvin’s misconception.
But you’re missing my point, which is that most of that variation (don’t forget T-cell receptors, btw) comes from recombination, not mutation.
Where does the theory say that “a change in the genetic code” should produce a new structure? As I already pointed out to you, almost all new biological structures are actually modifications of existing ones. There are plenty of examples of mutations altering existing structures, which is what the theory says. If that’s not what you’re asking for, then what are you looking for?
But that’s pretty much how morphological structures appear to be related: via modification of previously existing mechanisms/pathways and changes in the location and expression of pathways. Bithorax affects the development of body segments, resulting in extra legs or wings (plus internal structures). This shows how little genetic change is actually required to significantly alter morphological forms.
Based on what we know of developmental biology (functional and comparative) we don’t expect that kilobases or megabases of completely de novo DNA sequences are required to modify a fish fin into a leg and foot or a mammalian paw into a whale’s fin. Or modify wrist bones in pandas to allow better gripping.
I looked up “Mutation” on Wikipedia and it said some types of mutation come from recombination. How come their definition is so different from yours?
Mismatch repair at the end of recombination can generate mutations, but I’m not sure that it is true for antibody gene rearrangements. Either way, how does that suggest that the definitions are so different?
My point is that recombination generates more genetic diversity than the mutations.
Recombination in antibody diversity creation is mutation, Ben. It’s putting sequences together in a particular order that wasn’t originally present in the genome. Anything that changes a specific sequence is a mutation.
It depends on the recombination event. If we are talking about cross over events during meiosis then most geneticists would not consider that to be a mutation. In the case of antibodies, those would be somatic mutations, and random ones at that (with respect to antigen binding). Homologous recombination can also produce new genes, duplications, and so forth which can be heritable and are considered mutations.
Somatic hypermutation is really not “recombination.” It’s molecular vandalism followed by error-prone repair. The process is literally the creation and harnessing of random mutation.
[quote=“T_aquaticus, post:69, topic:36626”]
If we are talking about cross over events during meiosis then most geneticists would not consider that to be a mutation.[/quote]
And yet it’s a huge generator of genetic diversity because it puts “sequences together in a particular order that wasn’t originally present in the genome,” perfectly fulfilling Argon’s definition. Maybe you can explain that to Argon.
Moreover, if recombination in meiosis is defective, meiosis I fails and we get nondisjunction. It’s literally required for holding the maternal and paternal chromosomes in place.
[quote]In the case of antibodies, those would be somatic mutations, and random ones at that (with respect to antigen binding).
[/quote]They begin as somatic rearrangements that are regulated.
Duplications and deletions are mutations, yes. But everyday meiotic recombination, which generates massive diversity, is not.
Now, if we did WGS on the entire parental population of lizards and the entire population of the lizards that were transplanted, would we find new alleles from mutations that are absent in the parental population, or would we find new haplotypes generated by meiotic recombination, along with changes in existing allele frequencies?
No combination of modern human alleles is going to produce a giraffe, yet we evolved from a common ancestor shared with giraffes. Obviously, there has to be another mechanism.[quote=“benkirk, post:71, topic:36626”]
They begin as somatic rearrangements that are regulated.
[/quote]
Just as the roll of the dice or a shuffle of the cards is regulated.[quote=“benkirk, post:71, topic:36626”]
Duplications and deletions are mutations, yes. But everyday meiotic recombination, which generates massive diversity, is not.
Now, if we did WGS on the entire parental population of lizards and the entire population of the lizards that were transplanted, would we find new alleles from mutations that are absent in the parental population, or would we find new haplotypes generated by meiotic recombination, along with changes in existing allele frequencies?
[/quote]
We can also find instances where the emergence of new phenotypes was not due to shuffling of already existing alleles. For example, the emergence of dark fur color in pocket mice is associated with mutations in a gene known to change fur color, the Mcr1 gene.
http://www.pnas.org/content/100/9/5268.full
In this case, the dark fur allele is strong selected against the light brown desert. You only find that allele in black basalt outcrops that appeared relatively recently in the history of pocket mice. The dark fur allele is only found in the populations on the black basalt rocks, even though the dark allele is dominant. It is so strongly selected against in the light brown desert that you can’t find the allele at any appreciable distance from those islands of black basalt.
[quote=“T_aquaticus, post:72, topic:36626”]
We can also find instances where the emergence of new phenotypes was not due to shuffling of already existing alleles.[/quote]
I don’t see how finding 0/42 mice carrying the allele establishes that its allele frequency was zero in the ancestral population. Do you? If so, please explain statistically.
No, it’s associated with particular alleles. The paper didn’t show whether the allele was present in the ancestral population.
Yes. Do you think I would disagree with that?
[quote]You only find that allele in black basalt outcrops that appeared relatively recently in the history of pocket mice. The dark fur allele is only found in the populations on the black basalt rocks, even though the dark allele is dominant. It is so strongly selected against in the light brown desert that you can’t find the allele at any appreciable distance from those islands of black basalt.
[/quote]Not finding the allele in only 42 mice is not looking hard enough to establish that it’s not there. There are dozens of loci involved in pigmentation and they looked at two.
How about answering my question? What do you think we’d find if we did WGS on all of the lizards in both groups?
There are actually two black basalt islands, and black fur evolved different on each island.
The black allele is strongly selected against, meaning that the black basalt islands would have to exist before the black allele could be selected for. Since the black basalt islands are relatively recent additions to the light brown desert, it means that the mutation had to occur spontaneously.
That’s what alleles are, mutations.[quote=“benkirk, post:73, topic:36626”]
How about answering my question? What do you think we’d find if we did WGS on all of the lizards in both groups?
[/quote]
I have no idea. We could find brand new mutations or combinations of alleles found in the parent population. I don’t see how it matters if the mutation occurred prior to the selection pressure or after it.
Glipsnort…Again your preexisting structures don’t get a free pass. Where did those come from? You can go all the way back to the origin of life and you still would come up with nothing. Mutations may alter (slightly and occasionally) existing structures but these types of alterations do not add information or add new structural novelty. But if you have an example in mind that you think refutes this notion please present it.
Perhaps you could give us an example? What structures do humans have that other primates do not have? If you can’t find a structure specific to humans, then are you fine with humans sharing a common ancestor with other primates?
[quote=“T_aquaticus, post:74, topic:36626”]
That’s not statistical. Epistasis has not been eliminated as a possibility. There are almost 100 loci, and they looked at two.
The claim of it being selected against is a conclusion, not data. Why would positive selection be required?
I see that as a mere assertion.
me: No, it’s associated with particular alleles.
Not in genetics. Alleles are different versions of genes with different sequences. A mutation is the actual event that changes the sequence. IIRC, we are discussing how we know when alleles are preexisting vs. new.
The term you’re looking for is “mutant allele,” which is fraught with baggage, particularly in clinical genetics. If you don’t know which allele was ancestral, you really don’t know which allele is mutant, correct?
[quote]I have no idea. We could find brand new mutations or combinations of alleles found in the parent population. I don’t see how it matters if the mutation occurred prior to the selection pressure or after it.
[/quote]It matters a great deal educationally and politically, as this is at the heart of so much misunderstanding of Darwinian evolution.
Darwin never mentioned mutation and didn’t know what mutations were, but that doesn’t present polemicists from stapling the term “mutation” with all its silly baggage (for example, from X-Men films) for laypeople, all over Darwin.
Evolution is much less threatening if you approach it the way Darwin did: organisms in a population differ (fact), at least some of those differences are heritable (fact), so natural selection is common sense.
Do you not see why polemicists are so eager to shift the focus to “random mutations” instead of engaging with what Darwin actually wrote?
Epistasis has not been supported by evidence.[quote=“benkirk, post:77, topic:36626”]
Not in genetics. Alleles are different versions of genes with different sequences. A mutation is the actual change in the sequence. IIRC, we are discussing how we know when alleles are preexisting vs. new, correct?
[/quote]
Right. The differences between alleles are the mutations.[quote=“benkirk, post:77, topic:36626”]
IIRC, we are discussing how we know when alleles are preexisting vs. new, correct?
[/quote]
All alleles were new mutations at one point.[quote=“benkirk, post:77, topic:36626”]
It matters a great deal educationally and politically, as this is at the heart of so much misunderstanding of Darwinian evolution.
[/quote]
I care a bit more about science than politics.
The misconception in this thread is that mutations can’t produce new structures. What it boils down to is the assertion that changing the DNA sequence of a genome can not produce physical changes in the species. Pointing to the fact that sequence differences between alleles are responsible for changes in species meets that challenge, at least in my view.
your theory says we came not only from primates but from fish-type creatures and before that, bacteria-like creatures. Fish and bacteria don’t have knees or ball-and-socket joints, etc. Pretty much all you see would require additions of information and anatomy from simpler lifeforms.
So do you accept that part or not?
Hi Tom,
I didn’t set up the reply properly, but I’d be interested to read your thoughts on this earlier post:
“Let your conversation be always full of grace, seasoned with salt, so that you may know how to answer everyone.” -Colossians 4:6
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