Hmmm. Inversions can, you’d just need a huge amount of very localised recombination. Indels and duplications could be considered as merely deletions and deduplications from an original genome that contained the maximal contents.
True - there’d only have been three original versions. Well spotted.
Evidence for this claim?
Just looking at HLA genes, there are 6,000+ HLA A alleles, 7,000+ HLA B alleles, 6,000+ HLA C alleles, and so on. You can check it out here:
http://hla.alleles.org/nomenclature/stats.html
You need evidence for this claim.
The problem is time. There is about one recombination event per chromosome per generation which isn’t a high enough rate to produce the genetic variation we see in the short YEC time scales.
Then how in the world do we have different species? What make a dog different from a cat? The current understanding in biology is that the difference between species is due to a difference in the DNA sequence of each species’ genome. According to you, there should only be a single genome in existence and any deviations from that single genome can’t produce any type of beneficial changes. This would apply to all changes, even those allegedly made by God.
A mutation is any heritable change to the DNA sequence of a genome. They are mutations. You would also need to demonstrate how they are pre-programmed to make specific beneficial changes and what those algorithms are.
It’s also well known that those are random mutations. Those processes have no way of knowing if the changes they are making will be neutral, beneficial, or detrimental.
I suspect these beatings to be similar to my own explanations of the subject, provided to SFT directly on YouTube. I also suspect that SFT would ignore them in an identical fashion to mine.
You are cherry-picking.
You are suggesting that the present diversity in human alleles is because of a miraculous hot spot of mutations.
This hot-spot must be very broad in its spot… because there are several phenotypical traits with massive diversity in the current human population.
Even ID proponent Professor Bugg did not endorse such an analysis. Your view is practically anti-science if even Bugg finds it unlikely.
@SFT, I believe I’ve said something similar in terms of being able to have a productive conversation.
I only know enough population genetics to be dangerous, so I heartily invite the experts to pick apart the rest of this post.
The sudden affordability and availability of genome sequencing has produced a lot of data. Databases list tons of SNP’s and variants for different human genes. At least to my eyes, this simple fact destroys the case being made for a recent single ancestor for the human population.
Blood types was mentioned earlier, so that led me to look up a human hemoglobin gene as an example.
Just looking at the missense mutations (i.e. mutations that change an amino acid) there is a known variant at almost every position. I don’t see how all of these variants could be held in just two alleles due to basic functional constraints and epistatic effects. These variants have to be mutations, and I don’t see how these mutations could have appeared in the YEC time line and population model.
Let’s use 6,000 years since Adam and Eve and a generation time of 25 years which would give use 240 generations between any living person and A&E. Let’s say there are 100 mutations per generation which would give us 24,000 mutations in any given direct lineage. Sexual recombination probably has some effects here, but I can’t imagine it would change anything by orders of magnitude (please correct me if I am wrong). 24,000 mutations spread over a 6 billion base diploid genome isn’t going to produce that many mutations in any single gene, and yet we see tons of mutations in a single gene after sampling a small percentage of the human population.
Is my thinking correct here?
Nice to see some new names on the forum
And it can’t explain the divergence between alleles, which is what pushes the TMR4A so far back.
" 3) Some human genes have over 800 variants: These are the exception to the rule and you are probably referring to a subset of the immune system genes that are designed to change rapidly. Most common variants actually come in 2 versions. An exception might be the ABO blood alleles, but the most common version of O is clearly a mutated version of A, so it looks like there were two originals, A and B [see Blood types and their origin]. O must have entered the human population early, definitely pre-Babel and possibly pre-Flood. So, yes, Adam and Eve could not carry more than four alleles per locus among them (assuming God did not pack multiple different genomes into Adam and Eve’s reproductive cells), but the bulk of the genetic variation discovered to date could be fit into Adam alone (thus, the prior assumption seems valid). Add post-Fall mutations to the mix and I believe we have a good explanation of human genetic history in Genesis. See “Noah and Genetics” article referenced above"
Why don’t you name a gene and let’s see how many known variants there are.
These questions:
“The average human carries 4–5 million heterozygous
alleles,8
with Africans generally having higher levels.9
Is
it reasonable to assume the majority of these alleles were
placed by God into Adam and/or Eve? Would not most of
that initial created diversity have been lost at the Flood? How
much drift and/or fixation would one expect in a Creation/
Flood/Babel scenario? Would not the inbreeding of the three
post-Flood families drive humanity to extinction? Should we
expect genetic homogeneity among the descendants of the
Flood survivors, and is not the lack of homogeneity proof
that the Flood never happened? We can answer each of these
questions directly using computer programs that incorporate
real-world rates for various genetic phenomena (mutation,
chromosomal recombination, etc.).”
have all been answered.
Are you assuming all alleles are the result of mutations over time? How much created nuclear DNA heterozygosity are you starting with?
So you’re not familiar with the TMR4A work at all, despite saying earlier that you were confident it wasn’t a problem for your model.
Initial created nuclear DNA heterozygosity followed by post-flood and post-Babel mutations can easily explain the data. Many of these variable positions are designed to mutate for adaptive purposes.
" Is it possible for the two people of the Creation account (Adam and Eve) or the eight people on Noah’s Ark to give rise to all of the ABO blood types present in humans today? If Adam and Eve were heterozygous for blood types A and B, respectively (one allele for type O and one allele for either type A or B), they could have produced children that had any of the ABO blood types, as illustrated in Figure 2. The Punnett square simply predicts what the possible phenotypes would be for a given couple’s children. From the number of children that Adam and Eve likely produced, it is not difficult to envision all of the ABO blood types being passed down to their offspring.
If Adam and Eve were heterozygous for the ABO blood type gene locus, then the allele frequency for the type O allele is 50 percent (2 of 4 alleles), the allele frequency for type A is 25 percent (1 of 4 alleles), and the allele frequency for type B is 25 percent |Figure 2|. If there are no selective pressures or genetic drift for these alleles, then the allele frequency will remain constant through all of their descendants. The overall allele frequency in the Punnett square is actually the same for the children as it might have been for Adam and Eve. This scenario would also be true for Noah’s family and their descendants.
Modern Allele Frequencies
Do human populations today reflect these allele frequencies? The answer is yes. Table 2 shows the allele frequencies for several populations. (Note that these are not blood type frequencies.) There is a general increase in the frequency of the type O allele, and in many populations a drop in the type B allele. But as expected, the frequencies for each allele are close to what they could have been at the start of human history or with Noah’s family. The shift in frequency (the increase in type O and decrease in type B) can be caused by migration of people groups that had a higher or lower frequency for one of the alleles at the time of migration. It could also result from random genetic drift, or from a mutation that renders glycosyltransferase inactive–which would result in blood type O from type A and is likely one cause for the increase in the frequency of the O allele.
Unfortunately, the origin of the ABO alleles gets more complicated when examining the actual gene for glycosyltransferase. There are more than 180 variations (polymorphisms) for the ABO gene listed on the National Center for Biotechnology Information (NCBI) website,5 and each one of these polymorphisms can be assigned to one of the three ABO alleles. Most of these polymorphisms do not change glycosyltransferase activity or blood type, but can identify ethnic groups that formed after humans migrated across the globe. Mutation and chromosome crossing-over events are the most plausible cause of these variants.6"
How?
Based on what evidence?
By the way, there are over 1,000 variants (synonymous and non-synonymous SNP’s) for the ABO gene.
Its like you don’t even read the sources I provide. I have noticed this is very commonplace among this specific group in this specific post. If my sources are not going to be addressed and 99.9% of what I say is ignored I see no profitable reason to discuss this any further until what I have said is actually addressed in an honest way. I think this discussion speaks for itself as to who is presenting the data and who is providing smokescreen and incredible dodgeball skills.
You need to present the evidence in your sources. For example, where is the peer reviewed scientific paper demonstrating how all of the current human genetic variation could arise in just 6,000 years with a severe genetic bottleneck 4,000 years ago, and what is the evidence that supports their conclusions? Next, where is paper demonstrating that the ABO gene is designed to adapt. I have yet to see any evidence for adaptive mutations, whereas there is tons of evidence for random mutations.
“Mutation and chromosome crossing-over events are the most plausible cause of these variants.6”
I have also yet to see any testable predictions coming from anybody criticizing the young earth creation model here. There are many testable predictions in print ready to be tested in the lab by young earth creationists…except nobody on the evolution side is actually stepping up to the plate. Shame. Could be a lot of fun.