I have to tell you, I grow weary of putting the time and effort into addressing your claims only to have you ignore most of it and for you to then just reiterate the same bogus unsupported crap.
my questions in RED
1. You claim RM/NS is not fast enough to account for human evolution.
yes, I would claim that..
Yes, I know you would because you did and have been doing so for years.
Wait - are you claiming that you 'answered my question' by just restating it?
..............would you claim the opposite?
Yes, because the actual evidence says so. You just reiterate unsupported assertions with no rationale at all - just like you just did.
would claim that there is enough time for RM and NS to account for the evolutio of the human line?
Would I? Yes - because there is clear evidence that humans DID evolve from a common ancestor with chimps.
, would you atleast admit that this is an open question that is currently being evaluated by scientists?
No, because at best, what fringe types like Muller are claiming is that other factors - other GENETIC factors - may be involved. As I wrote before, however, the claims of people like Muller are not taken as a given, there are many that disagree with them.
2. I ask for evidence for this, you eventually declare nonrandom mutations like transposons make it fast enough, even though you don;t believe it anyway
All I am saying is that transposons likely played an important role and are responsible for some of the “evolution”
Why do you say that? And why did you bring them up in the context of the 'speed' of human evolution?
Did you not read my treatment of transposons being nonrandom?
Will you at least admit that your 30 million number is inapplicable and that your totally unsupported claim that most of those must be beneficial is based on nothing but a desire for it to be so?
This mechanism can produce new proteins in just 1 generation so yes under that basis the mechanism is “fast enough “
In
one organism, yes - just like a mutant allele can also make new proteins in just one generation, but it still has to spread under the same constraints as any other mutation event. You do understand that, no?
Well, actually, it is obvious that you do NOT understand this.. Surely you are not implying that a transposon inserts into ALL members of a population in 1 generation???
Do you understand NOTHING about how these things work?
Under your view, did transposons play a major role?
Major? That is a subjective position to take, but I would generally say no more than any other mutational event.
Any evidence to the contrary? I do think I know where your confusion comes from (though you probably read some inaccurate propaganda on a YEC site and ran with it) - there seems to have been an increase in transposable element activity within the human lineage in the last 4 million years or so relative to other primates that produced selectable changes, thus making them more readily selected for (beneficial mutation rates are dependent upon, among other things, the initial occurrence of the mutation and the population size), at least according to 1 2011 paper. But transpostion is still a mutation even, a genetic event, not something magical. And, again, even such changes/insertions with high selection coefficients still have to spread in a population, they are not universal "in one generation".
Will you at least admit that your 30 million number is inapplicable and that your totally unsupported claim that most of those must be beneficial is based on nothing but a desire for it to be so?
3. I remind you that a transposon still has to spread through a population like an SNP has to, and ask how this would speed things up. You ignore it.
Yes but transposons can produce new functional and selectable proteins (genes) in 1 generation…
Just like RMs. Your point? Do keep in mind that this may occur in but a single individual, so it still has to spread, and just because they can contain their own genes, it is a mistake to conclude they all do.
….the RM+NS model would require a gene duplication + thousands of point mutations in order to get something that we would call a “new gene”
Wow...
I'm sorry but you really need to take a class in genetics.
1. Gene duplications in and of themselves can produce selectable changes, even without subsequent mutations. See 'HOX genes'.
2. A SINGLE mutation in one gene can produce large-scale phenotypic changes.
3. Since the average exonic portion of a gene is around 1500 bases, you are suggesting that most or all of the nucleotides within a coding gene have to be changed to produce a new protein. Evidence for this please?
4. Not all phenotype-altering changes need to be in genes, but can also be in regions controlling gene expression. So again, no huge number of mutations within genes is required.
5. de novo genes are a thing, and they do not require 'thousands' of mutations:
Origin and spread of de novo genes in Drosophila melanogaster populations *
"We identified 142 segregating and 106 fixed testis-expressed de novo genes in a population sample of Drosophila melanogaster.
These genes appear to derive primarily from ancestral intergenic, unexpressed open reading frames (ORFs), with natural selection playing a significant role in their spread."
6. Will you at least admit that your 30 million number is inapplicable and that your totally unsupported claim that most of those must be beneficial is based on nothing but a desire for it to be so?
4. then you claim as support that RM/NS is not fast enough.
No, the claims that I would use to support is that traspososn (and other mechanisms) can generate big genetic changes in a small amount of time, meaning that this mechanism can account for the fast rate of evolution.
Please tell us all about the "big genetic changes" that can occur as a result of transposon insertion in "a small amount of time". How big is the big genetic change? And how small is the small amount of time? And do you not realize that if we take your word for these effects, that you are actually helping the evolution cause given your constraints put upon it?
Can you show that the mechanism of RM and NS is “fast enough” under what basis?
I already showed that plain old RM and other known genetic phenomena can account for the 30 million number you dreamed up. That a certain proportion of those may have been adaptive is a given. Given that it is established that small, even single genetic changes (SNP) can produce large phenotypic effects, and that the traits that humans possess are modifications of already-present traits in even basic mammalian precursors, much less Primate ancestors, there is no real scientific reason to believe that it was a necessity for some untold huge number of beneficial mutations to have been required to get a human from an ape ancestor. That is mere emotional rhetoric, often couched in bogus genetic presumptions and bogus calculations.
Creationists are unable to provide evidence on the number of beneficial mutations that were required for even 1 trait, nor how many such traits need to be accounted for - why do they expect their assertions that have no rationale or scientific basis to be taken seriously?
5 million years is not enough time (for what???)
not enough time For 30M beneficial mutations (or something close to 30M) To have occurred, become selected and fixed in the population.
Beg the question much?
Please provide a rationale or better yet, evidence, that such a large number of beneficial would have been required.
As that is your claim, provide the evidence.
I understand that you would say that this is a strawman, so would you provide the correct numbers?
I have written to you on at least 3 occasions that I can remember that I have no idea. I am not claiming that I DO have the number, YOU are.
First, you stole Remine's number. Then you apparently stole Sanford's use of ReMine's number. Then you applied simplistic math and just declared that each and every nucleotide difference between human and chimps must have been beneficial.
Yet not one of you - not ReMine, not Sanford, not you - have ever offered any kind of reason or rationale for claiming this need of large numbers of beneficial mutations, much less an attempt at providing evidence.
It would be like me claiming Jesus wasn't strong enough to carry the cross so the crucifixion story is fake, but never being able to provide data on the size and weight of the cross.
2. Nonrandom mutations somehow spread faster through a population than SNPs.
yes that is what I would say ..
Yes I know, but you cannot seem to provide any evidence for it.
.None random mutations are more likely to be positive,
Evidence please.
more likely to be selected for,
Evidence please.
more likely to build complex stuff like complete proteins) in a single generation
Evidence please.
, this is why the would spread faster than random mutations.
And Jesus could not carry the cross because He was too short and weak, the cross was too large, the wood the cross was made of was too heavy, his shoes did not offer enough support.
That is why Jesus could not carry the cross.
Ask me for evidence for this? Sure -
Jesus could not carry the cross because He was too short and weak, the cross was too large, the wood the cross was made of was too heavy, his shoes did not offer enough support.
That is what it is like discussing this stuff with you.
Not one thing you wrote supports your claim that transposons spread faster in a population than a similarly beneficial SNP.
As an analogy you can go from point A to B faster if your steps are intended towars that direction, than if you just make random steps towards random directions.
And if one of those random steps is in the right direction, it would be selected for. Just like a TE insertion.
So again explain how a transposon that confers an advantage spreads more rapidly though a population.
mammals and particularly the human line evolved too fast "
Yes, they evolved too fast to be explained by RM and NS that is what I would claim
You want evidence Jesus could not have carried the cross?
Here it is:
He was too short and weak, the cross was too large, the wood the cross was made of was too heavy, his shoes did not offer enough support.
, is there any academic source that concludes otherwise?
If yes, can you present that source?
Why do you never have to present evidence for your claims? When YOU provide 'academic' support for any of your claims, I will endeavor to support mine (even though in this thread alone, I have linked to and/or quoted about a dozen such sources in support of my claims, and you have done the same for... NONE).
If not, then why are so affirming with a seemingly high level of certainty that RM and NS are fast enough?
If not, then why are you claiming that all 30 million differences had to be beneficial, there is not enough time anyway, and transposons spread in a population faster than other kinds of mutations?
I no longer feel compelled to do anything more than write assertions, since that is all you seem capable of on any topic.
