“The data” isn’t a link to data. It’s just an assertion at the end of a sentence. You have brought no data, I have. What you say contradicts the data I have brought. That means when you say my arguments contradict “the data” you are in denial of the data.
Get your denial under control.
This combination of the trivially true but irrelevant, the incoherent, and the outright false is, IMHO, peak Bill. The creationists only send us their best.
Bill the core in globular proteins is hydrophobic (it needs to be generally nonpolar to repel water and show mutual attraction), not hydrophilic. And funnily enough Axe showed the core of globular proteins is fantastically tolerant to mutations.
Yet another topic about which you know not even the slightest thing.
This is true Rum but it does not help the fact that there is no model that supports the various Venn diagrams.
If you really think you have a chance with this engage an expert and build a real model like the Behe/Lynch models. My prediction why this will not happen is because of trying to model so many changes, reproduction rates, realistic mutational outcome, gene duplication rates, deleterious nature of multiple gene losses, and deleterious nature of chromosome mutations.
Not a single thing about chromosomal fusions in that article. Data not relevant. It’s about parts of chromosomes changing locations to other chromosomes, parts internal to chromosomes inverting, entire chromosomes or large parts of them being deleted, or having multiple copies of the same chromosome.
No fusions or fissions.
You still have not brought data. You are still in denial of the data.
From the article.
Robertsonian translocations occur at or near the centromere of chromosomes 13, 14, 15 and 21, and 22 that have very short arms already. The shorts arms fuse and the long arms form a much larger chromosome (Figure 2). Often the overall chromosome count is reduced from 23 to 22 because of this. It occurs in about 1 in 1,000 live births without phenotypic changes or heighted disease risk (40). However, it does raise the risk of trisomy in any offspring, particularly Down syndrome
That’s not a telomere-telomere fusion. Incidentally even Robertsonian fusions can often have no phenotypic effect.
Translocations
Translocations result in re-arrangements of the chromosomal material. These can be balanced or unbalanced translocations depending on even or uneven shifting of material (Figure 2). Balanced translocations essentially switch material between chromosomes without any loss or gain of genes and therefore causes no negative imprint or phenotype for the affected individual. These occur in about 1 in 500 births (39). Though typically healthy, these carriers have a higher risk of creating unbalanced translocations in their gametes, which would then be passed on to their child. In an unbalanced translocation, genetic information is exchanged unevenly such that there are either extra or missing genes. A less common exchange is non-reciprocal, in which material from 1 chromosome moves to another, but no material comes back to the first.
The vast majority of fusions in deer are tandem fusions(telomere to telomere).
Here is a paper that includes the deleterious nature of tandem fusion in deer. They are arguing for reproductive isolation but how would you model if this is a viable explanation?
From the other paper I cited.
Chromosomal abnormalities are relatively common in men with infertility. Therefore, men with azoospermia, severe oligospermia, or clinical phenotypes suggestive of chromosomal abnormalities should have a karyotype performed. Treatment varies pending the results of the chromosomal analysis.
Where does it do that?
It’s what the paper is basically about.
Conclusion
Lineage A- Paraná and Lineage B- Juína) possess an efficient mechanism of post-zygotic reproductive isolation, which involves infertility or subfertility of the hybrid. Once the true impossibility of gene flow between the lineages is identified, more concrete discussions on modifications to the taxonomy of this species can be initiated. In light of the results of this study, combined with previous studies, both lineages may be considered as cryptic species that present the same phenotype. Populations with similar karyotypes must be evaluated more carefully, since there is a reasonable likelihood that they are also distinct species. Chromosomal changes have proven to be an efficient and powerful mechanism in the isolation of populations and in the formation of species in the genus Mazama.
In this study, we verified that two of the six chromosome variants that exist within M. americana (
That’s once again attempts at hybridization between two considerably diverged populations (the A and B lineages). The paper argues that chromosomal rearrangements accelerate speciation because as two separate lineages independently accumulate chromosomal mutations, their mutual compatibility rapidly decreases as the hybrids are more likely to be infertile or have subfertility the more different the lineages are. So gene-flow between the two lineages drops off, they diverge, and eventually speciation has occurred. It doesn’t anywhere say that individual chromosomal mutations can’t accumulate over time in separate populations.
I completely agree but if you are at all skeptical that these distinct species were caused by random reproductive mutations causing isolation you will note a strong deleterious nature of chromosomal change in a population must be included in a model based on the empirical evidence.
So now you’re back to just asserting that chromosomal fusions are all or in the vast majority of cases strongly deleterious. Despite NONE of your papers showing that.
And I have brought a paper that directly test that by engineering chromosomal fusions into a mammal and finding the vast majority have no measurable effect.
In conclusion: You don’t read your own sources for comprehension. You persist in denying the data.
You are misread the papers.
If an offspring has a mutation where it cannot regularly mate with the existing population this is a highly deleterious mutation as their relative fitness is substantially less then the non mutant deer in the population.
Where correlation does not necessarily equate to causation it is an indication of causation.
No, you misread the papers. There is nowhere in any of the papers where it shows that telomere-telomere chromosomal fusions, individually, typically cause infertility. ALL of your papers show work where hybrids produced by matings between much more diverged lineages that each have multiple chromosomal differences (not limited to telomere-telomere fusions) already accumulated, have reduced fertility or are infertile.
Read your own sources with comprehension. That means to understand what they are saying. Read them to understand what they say so you can also understand what they don’t say. That is to say, understand their limitations.
Some chromosomal mutations are deleterious =/= all or the majority of chromosomal mutations are deleterious.
Already diverged lineages each with multiple(several more than one) chromosomal mutations of multiple types, coming together to produce hybrids often results in infertile hybrids =/= a singular telomere-telomere fusion, or a singular balanced Robertsonian fusion, also typically produces subfertile or infertile hybrids.
The latter does not follow from the former. Fathom it. Understand it. Realize it. Deal with it.
C O M P R E H E N D.
What is the chromosome difference between and infertile mule and and a horse and a donkey. The answer is a single chromosome mismatch. You need to be able to read these papers and integrate with other data we know about infertility. A single chromosome mismatch can can be deleterious to a population.
This is what you need to demonstrate to support your model. The current overall data does not support this assumption.
There is nowhere in any of the papers where it shows that telomere-telomere chromosomal fusions, individually, typically cause infertility.
Let’s look for key words:
There is nowhere in any of the papers where it shows that telomere-telomere chromosomal fusions, individually, typically cause infertility.
And your statement is false. Horses and donkeys have numerous chromosomal differences. They have one difference in the number of chromosomes, but 9 of them have considerable morphological differences as well.
Summary
The diploid chromosome number for Equus caballus is 64, that for Equus asinus is 62, and that for the mule, 63.
The chromosome complements of E. caballus and E. asinus are completely different morphologically. E. caballus has 19 pairs of metacentric autosomes and 18 pairs of acrocentrics, while E. asinus has 19 pairs of metacentric autosomes and 11 pairs of acrocentrics. The morphology of the sex chromosomes is also dissimilar between the species.
While the disparity between parental chromosomes satisfactorily accounts for sterility in male hybrids, it does not explain the occasional fertile female able to produce several offspring with no
E. asinus traits. Apparently morphological disparity between parental chromosomes is only a small part of the relatively complex matter of female gametogenesis.
You are extremely confused. When I say some does not equal all, I am saying you cannot infer that because SOME mutations are deleterious that therefore ALL mutations are deleterious. That’s an invalid inference.
Comprehend?
So, Bill, that statement isn’t an assumption, it is just a statement of inequivalence. It means the two statements on each side of the not-equal symbol(=/=) are not equal. This isn’t something that needs to be proven. If this is not self-evident to you then you should be calling 911 as you may be suffering a clot in the brain.
Some just aren’t all. So what I mean to imply by making that statement is that the latter statement
does not follow from the former statement
That’s not an assumption I’m making. That is an elementary logical deduction. The negation of the deduction commits a fallacy in logic.
Can you please show signs of understanding? Just a small sign that something is beginning to click. Bricks falling into place.
Your claim is chromosome mutations are neutral for your model. This is obviously false at this point.
They eventually cause infertility when hybridization occurs in the population from chromosome mutations. Remember the paper posted on mice hybridization. 22 and 24 mated chromosome variants cased infertility in the female and sterility in the male.
You are building the model Rum and your statement needs to move from conjecture to a quantification of non deleterious chromosome mutations in the deer population due to chromosome change.
Lets replace All with most.
I have not seen any data that shows that variants in chromosome counts from the wild type can become fixed in a global or regional (country) population. Although the inference is tentative it is not without reason.
I don’t claim they all are. They don’t all need to be for the rate of fixation to be close to the neutral rate. There just needs to be some fusions that are neutral for those to go to fixation at appreciable rates.
In one of your own sources they say balanced translocations (which have no effect on phenotype), for example, occur at about 1 in every 500 births. That’s a very high rate, so a LOT of balanced translocations could in principle fix in a few million years. I have already brought a paper that shows the majority of telomere-telomere fusions engineered in mice had no measurable phenotypic effect. Those too would behave as neutral mutations and thus have no problem fixing at the same rate they occur.
Again you have failed to comprehend.
So singular telomere-telomere fusions, or balanced robertsonian fusions, mostly cause infertility? Where’s the paper that shows this?
What paper? Don’t mention a paper without linking it. Yet another one that doesn’t say what you want it to?
Surely you’re not thinking of the paper literally titled “Measurement of hybrid fertility and a test of mate preference for two house mouse races with massive chromosomal divergence” instead of just a single telomere-telomere fusion occurring in the same population?
You need to try to fathom this idea that within a single genetically more homogenous population, an individual with a single telomere-telomere fusion, is a very different thing than having two already diverged populations with significant differences in chromosomal numbers and morphology coming together to produce a hybrid. Not equivalent situations.
I have. They occur at high rates and most have no measurable effect. Remember the paper where they engineered them in mice?
Same fallacy. Some =/= most.
Jesus Christ, dude.
Mice. You have seen the data on mice. n=22 vs n=40. Are you saying different subpopulations of mice were independently created again?
Bill it’s just a rate of fixation of neutral mutations, which would be equal to the rate of occurrence in a population of constant size. So for chromosomal fusions (which we know empirically are mostly neutral), you just take the rate at which they occur and then the mean rate of fixation is the mean rate of occurrence(there would be some variation around the mean of course).
Your model is treating them as neutral. They are not neutral and you are miles from quantification.
I am saying these subpopulations are small and show no real substantive evidence of fixation. If all Switzerland had fixation of say n=22 then you would have a comp to an individual deer species. The evidence for this is not available and does not bode well for chromosome changes not being highly deleterious to populations.
Translocations are the most common type of chromosomal structural anomalies. Chromosomal translocations are known to reduce fertility in men and women. A study of 1056 infertile men showed that 16.1% had chromosomal abnormalities and 2.1% had chromosomal translocation [5]. It has been reported that the reorganization of chromosome architecture, including ROB translocations, were 6–10 times higher among infertile males compared to the general population
https://doi.org/10.2144%2Ffsoa-2020-0037
Structural chromosome abnormalities are known to affect fertility rate in domestic animals. Checking these abnormalities is an important mechanism used to exclude from breeding programs to prevent the transmission of the undesirable traits contained in their genome [20]. Improving fertility traits such as litter size, entails mitigating the effects of embryonic loss during pregnancy. Chromosome aberrations have been known to increase the risk of embryonic malformations and early mortality in livestock [21]. To checkmate the negative impact of chromosome anomalies, a number of countries have developed cytogenetic screening programs, where animals intended for breeding are tested for chromosomes aberration and appropriate measures are instituted to prevent the economic losses associated with them. Such countries include France and Canada, both in the pork industry [22,23]. Breeding boars and sows are screened for chromosomal anomalies, with animals found with anomalies being culled from the programs. This resulted in the most precise estimate of the occurrence of chromosomal anomalies in livestock and in improving economic gains when animals with chromosomes aberrations are culled.