I would conclude that length is not important for these specific introns or there is design customization.
How do you explain needing specific intron length in developmental genes to properly build an animal could have originated from a step by step process?
If one could still be amazed byt the degree to which creationists are impervious to evidence and explanations, it would be amazing that they still believe the existence of Junk DNA is demonstrated by nothing more than absence of evidence for function.
Its based on an untested theoretical construct.
Based on what?
There is nucleotide bias in humans compared to other creatures. Is that an accident? No one knows.
It’s premature to say.
In anycase, to the extent that the extrusion loop configurations are cell type dependent, then structural length provided by introns is even more important, in fact it was easy to see from the examples above (like FIRRE), one can’t reasonably suppose large scale deletions or changes in positioning of loci is amenable to stable function.
Pffft.
You should be the last person to make this claim since 90% of the genome lacks sequence conservation, the feature you use to define functional information. Also, the conclusion that the human genome is mostly junk isn’t speculation because it is based on the evidence of sequence conservation.
So in other words you’d stick to your conclusion despite all the ways one would have of testing it.
He already explained that for forks sake. Some few are functional and show conservation evidence of being functional, and the rest are not, and the evidence for that is the lack of conservation.
What evidence would you need to see in order to conclude that most introns are junk?
What percentage of developmental genes require a specific length of intron? Percentages matter.
You need evidence to back these claims.
Not even high school geometry is need to see an extruding loop has to be long enough and in the right place to position a molecular machine.
Speaking of nucleotide bias affecting structure:
Nucleotide composition bias also influences local chromatin organization, with consequences for exon recognition during splicing. Interestingly, the GC content of exons correlates with that of their hosting genes, isochores, and topologically associated domains.
Changes in bias via mutation is therefore a slightly deleterious mutations (SDMs), exactly in line with the problems not only in John Sanford’s Genetic entropy but for that matter Kondrashov and just about every major geneticists who understands the danger!
How long is long enough? Why is a specific length of intron needed to meet that length requirement?
This makes no sense. Chromosomal domains are much larger than introns or even genes, such that at most one intron in a fraction of genes will contribute the information needed to define an extrusion loop. This is much, much lower than the very generous estimate I gave. (Even worse for your proposition, @stcordova, is that a given intron doesn’t need a hundred bp of specific sequence to participate in the extrusion process.) This cannot possibly add significantly to the overall fraction of function in intronic sequence space.
Actually, the paper that goes along with your video suggests just the opposite. The authors deliberately eliminated individual CTCF sites and showed the expected changes in large-scale architecture. But the cells that were subjected to these changes were still able to grow, such that the authors did not report any effects. (This is actually very important - any substantial physiological effects would dramatically change their conclusions.) Do you read any of the papers you cite, @stcordova?
(I will add upon further reflection that the idea that an extrusion loop may be anchored in an intron is itself a difficult one to reconcile with the other proposed functions for these loops. For example, wouldn’t this impede transcription through a gene that is anchored thusly?)
Look at rats and mice introns. If your hypothesis is right then there should be a lot of sequence variation and length variation due to fast generation times. You can start to test the hypothesis this way.
Still no evidence you need so many introns for that.
I am talking about YOUR hypothesis that most of the human genome is functional. What evidence would falsify that hypothesis?
This is not my hypothesis.
This may be yet another example of ID/creationists needing some experience in the lab. I and probably every molecular biologist out there have cut and then ligated plasmids back together. This requires one end of the DNA molecule to bend around and come close to the other end. There is no sequence in plasmids that is required for this to happen since DNA is a flexible molecule. It bends on its own. The bendy molecular gymnastics gets even crazier when you want to insert a short sequence into that gap in the linearized plasmid, and yet it happens spontaneously and without the need for specific sequence to bend the DNA.
So you agree that there is no evidence that a majority of the human genome has function?
Its is uncertain how much of the human genome has function. Your rhetorical games duly noted.