What exactly are you trying to hit at? its not clear at all.
Didnât you just give away the game? If youâre claiming that 3D elements are the true controlling features of development, you have just agreed that theyâre a consequence of DNA sequence and so changes to DNA are what produce changes in regulation.
Not true. Coding sequences are around 0.5% different, but junk sequences are only1.2% different. You also have entirely and consistently ignored the problem of nested hierarchy.
Okay, so itâs the genetic sequences, which are heritable, and can mutate and be subject to selection.
Glad we got this settled.
Of course that fact has been known since the dawn of genetics, as it was understood that non-coding DNA serves as binding spots for transcription factors. So-called promoter regions.
Non coding DNA (mostly actual junk in many species, particularly large multicellular eukaryotes with smaller effective population size) is often highly repetitive(thus intrinsically prone to large-scale deletion or duplication mutations due to strand slippage and unequal crossover during homologous recombination) and consists largely of both dead and still active transposons (which again contributes to the plasticity of genome size over evolutionary timescales)
That would be mutations. Mutations of all their types. Insertions and deletions, chromosomal inversions, duplications(unequal crossing over, strand slippage etc.), and substitutions. Basically there exist mutations of exactly all the types needed to change a genome both incrementally and ârapidlyâ. Total genome size can change up and down both due to large duplications, insertions, deletions, or transposon activity.
Didnât you just give away the game? If youâre claiming that 3D elements are the true controlling features of development, you have just agreed that theyâre a consequence of DNA sequence and so changes to DNA are what produce changes in regulation.
No, because genetics are not the only factor. What I am saying is that globally gene regulation itself doesnât change, only the genome can change. Also I am providing evidence that most of the genome is functional (more about that later). Since most most important traits are regulated by many genes most mutations are near neutral, with a few being mildly deleterious and a smaller number being mildly beneficial. However if random gene mutations begin to accumulate that impact gene regulation the result are harmful mutations. There are many examples of diseases causes by such mutations with Rett syndrome being.
I think if we take population genetics seriously then the high level of genetic sequence specific functionality that we see in the human genome demonstrates that a non teleological process of evolution could not have possibly occurred, unless it occurred by some still undiscovered process. In a 2017 paper one author used population genetics based calculations to declare that the part of the human genome that is functional in a gene specific way can not exceed 15%, as we can read here:
Which is interesting because as the papers that I highlighted yesterday suggest the evidence coming from direct observation is pointing in the direction that most of the genome is functional in a sequence specific way.
https://www.nature.com/articles/s41598-019-51036-9#Sec10
Not true. Coding sequences are around 0.5% different, but junk sequences are only1.2% different.
Not if we count structural variants, and most non coding sequences are not junk. I think counting structural variants we humans are 1.5% different from one another, but I canât find a hard number for the level difference between humans and chimpanzees that counts structural variants.
You also have entirely and consistently ignored the problem of nested hierarchy.
Itâs not a problem, because nested hierarchies are usually the result of organized thinking and standardization, not blind processes. Some examples are:
Social Groups:
https://www.nature.com/articles/srep06526
Computer Programs:
Economics:
Engineering
http://faculty.business.utsa.edu/manderso/STA4723/readings/Mason/ch11.pdf
And of course biology, just to name a few. This is why I am not as impressed with the nested hierarchy of life as you are because no one claims that it as evidence of blind processes except biologists. because I know that most nested hierarchies are the result of design constraints and logical thinking, it is only evolutionary theory that claims that nested hierarchies can only be the product of common descent, but this of course is not true as the above examples show.
So what do phylogenetic trees represent? They are diagrams cataloging the comparative structure of genes, amino acid sequences that have the same or similar functions under a range of physiological constraints on gene variation. Sometimes, but not always, these tree correlates to similarities in morphology and diet. However, I would add that an observable pattern does not demonstrate in and of itself that an unobservable process occurred. I think that the percentage the genome that used sequence based functions are too high to make an unguided process of evolution possible, although I would concede that a guided process would still be possible.
What exactly do you mean by âstructural variantsâ? And of course they are.
I donât think you still have any idea what a nested hierarchy is. Itâs what we expect from common descent with branching. Itâs not some index of organization. Whatâs organized about a bear that eats only bamboo, or a cow relative that looks like fish, or a possum relative that looks like a wolf?
Do you not understand why nested hierarchy is a clear prediction of common descent?
Genes are not amino acid sequences. Related genes often have different functions. Not sure what you mean by physiological constraints on gene variation, but thereâs a lot of word salad in that sentence. You should also know that lots of trees are not based on protein-coding sequences.
Well, of course the process is observable. But if we take that sentence seriously it invalidates all of science. Particle physics becomes useless, since the particles are all too small to observe directly and are detected only by patterns in data.
Your notion of the functional percentage of the genome is flawed. I direct you again to the onion test. Or if you prefer, you can try to explain the fugu genome. But why, even if you were correct, should unguided processes not explain it? Finally, given your last clause, why do you nevertheless reject common descent?
Sorry, but that makes no sense at all.
I direct you again to the onion test. Or if you prefer, you can try to explain the fugu genome.
What a ridiculously easy physics problem, I accept your challenge and will use your onion test to show how physics can be used to explain phenomena, in a way that has much greater practical value than using baseless population genetics based constraints, as a rationalization to call the onionâs large functional genome junk DNA.
I googled this problem and I almost canât believe this simple problem has not been solved! I think that itâs because everyone sees this as a gene expression problem when itâs actually a solution that protects the genome from being crushed by the high levels of mechanical pressure inside the onion cell. The solution that I will propose will not only explain why the onion genome has to be as large it is, but is applicable to understanding the role of polyploidy in plants that are not diploid. First letâs think a little about plants, some of the differences between plants and motile animals are:
- They are immotile with a cell wall.**
- This means that they do not pass through gastrulation or tissue migration.**
- Their DNA is still globally regulated by mechanical pressures just like animals.**
- Plants cells have a much higher level of internal pressure than animal cells, and they use this internal pressure to change cell shape by making modifications to their cell wall.**
- Onions are geophytes that form bulbs.**
First I will use a molecular biology textbook to explain how plants modify their cell shape. Please click the link below and look at figure 22-32.
https://www.ncbi.nlm.nih.gov/books/NBK21709/
Using this same reference I will discuss how the cell uses auxin to modify the cell wall and change cell shape, it explains:
Cell growth in higher plants frequently occurs without an increase in the volume of the cytosol. Because of the low ionic strength of the cell wall, water tends to leave it and enter the cytosol and vacuole, causing the cell to expand. A localized loosening of the primary cell wall, induced by auxin, allows the cell to expand in a particular direction; the size and shape of a plant are determined primarily by the amount and direction of this enlargement (Figure 22-33a). Individual plant cells can increase in size very rapidly by loosening the wall and pushing the cytosol and plasma membrane outward against it. The increase in cell volume is due only to the expansion of the intracellular vacuole by uptake of water. We can appreciate the magnitude of this phenomenon by considering that if all cells in a redwood tree were reduced to the size of a typical liver cell (â20 mm in diameter), the tree would have a maximum height of only 1 meter.
With this general principle in mind we will now consider Some of the unique mechanical pressures face by onions by looking at the onion structure, here is how one paper describes it:
In general, the fine structure of the onion cell was characteristic of a quiescent cell and some of the main features can be seen in Figure 2(a). The cells were very large and thin-walled with large central vacuoles, some of which were apparently empty whilst others were filled with a fibrillar material. âŚ
The flattened, peripheral nucleus was seen to contain a prominent nucleolus [Fig. 2(c)].
https://nph.onlinelibrary.wiley.com/doi/pdfdirect/10.1111/j.1469-8137.1981.tb03197.x
Since the central vacuole in the middle of onion cells and other geophytes is much larger than that of other plant cells, the onion cell nucleus is under much higher levels of pressure than many other plant cells that have smaller central vacuoles especially when this vacuole is full of water. So the large genome in the onion cell is used mostly to prevent these periodic increases in pressure from crushing the nucleus altogether, as would happen if the cells had a smaller genome like humans do. Based on the above physical considerations I would expect the genes in the onion genome to be separated by large intergenic regions and to be which would act as shock absorbers protecting the genes. Letâs see how this physics based prediction holds up.
All that I could find was one preprint article but I canât see why it would get the arrangement of the cellâs genome wrong it states:
Only 72.4% of the genome could be identified as repetitive sequences and consist, to a large extent, of (retro) transposons. In addition, an estimated 20% of the putative (retro) transposons had accumulated a large number of mutations, hampering their identification, but facilitating their assembly. These elements are probably already quite old. The ab initio gene prediction indicated 540,925 putative gene models, which is far more than expected, possibly due to the presence of pseudogenes. Of these models, 86,073 showed similarity to published proteins (UNIPROT). No gene rich regions were found, genes are uniformly distributed over the genome.
So if using our knowledge of how specific repetitive gene sequences control the relative firmness and flexibility of the chromatin as explained in the earlier paper that we read, I would say we have found found that 72.4% of the onion genome serves the specific function of osmotic pressure shock absorption in a nucleotide sequence specific way. So yes most of the onion genome is functional. What is more since all plants have central vacuoles the fact that plant genomes tend to be larger than motile animal genomes seems to be better explained by physics than by luck driven evolutionary narratives. Hereâs that paper again that challenges junk DNA:
https://www.nature.com/articles/s41598-019-51036-9#Sec10
I would suggest that junk DNA is an argument from ignorance, while physics not evolutionary theory is the appropriate tool to understand the real and discoverable functions of DNA sequences of unknown function.
Sadly, you seem not to have understood it. The question isnât why some particular onion genome has a different size from the human genome. Itâs why two closely related onion species, nearly identical in appearance, have genomes of radically different size. Nothing you say below is relevant to the onion test. Either your source misunderstood the test or you have misunderstood your source.
Edit: More generally, the onion test is simply an instance of the C-value paradox. Your âexplanationâ might conceivably show why plants have larger genomes than animals (if indeed they did, which they donât) but it canât explain the radical differences in genome size among plants (even accounting for ploidy).
It doesnât. You have misread that paper too.
I thought as much, but itâs nice to have the confirmation.
Thanks for what I am sure will be the biggest laugh I have today.
OK guys, letâs cut the mockery. Please edit comments appropriately or they may be hidden.
@Geremy you pretty much set yourself up to fail. I can protect you from mockery but not from being wrong. It would be good form to acknowledge an error.
Wild garlic has a haploid genome size of 30.9Gb, while chives have a haploid genome size of 7.5Gb. Both are diploid organisms. According to your model then, does wild garlic have significantly larger vacuoles than chives? You say intracellular pressures are larger in geophytes, but there are no geophyte gymnosperms and yet gymnosperms have the largest average genome sizes among plants, why is that? Some geophyte species have haploid genome sizes around 0.25Gb, why is that? Do you expect to see a general correlation between intracellular pressure and genome size? Does that mean deep-sea fish should have much larger genomes than closely-related surface fish?
Youâre being incredibly naive if you think you can look at differences in genome sizes between 2 species, notice that intracellular pressures are also different, and then confidently conclude that intracellular pressures must be the cause of the differences in genome size. You shouldnât dismiss the vast literature on plant genome size evolution.
I will concede that the problem is a little more complex than it initially looked like it was from a physics angle. I have found an animal example of the marbled lungfish that I will have to look into much more to explain from a pure physics perspective. I do think that physics seems to be able to explain the general pattern better than evolution can in most circumstances. I have found an example of a plant called the Paris japonica which only makes sense from a hybridization perspective.
Since hybridization is a form of evolution I will withdraw the claim that evolution is not the cause in some cases, especially of very large non diploid genomes. However I donât think that a few special cases invalidate the overall pattern which seems more consistent with it being physics that is driving the genome size, and more important structural differences, between animals and plants. That said I definitely do not as yet have the whole picture. I will need to compare the ability of onion species to dissipate pressure via secondary vacuoles and/or cell wall flexibility and other factors to either provide stronger empirical support for the main hypothesis, or falsify it.
That would entail that whatever mechanism you think of better predicts genome size than phylogeny does. Do you want to take bets on that?
Thatâs a start!
Single cases are sufficient to falsify hypotheses. It is not wise to call a case an âexampleâ without a much larger sample.
I donât, but then Iâm just a guy who spent two years on sabbatical in one of the best biophysics labs in the whole world.
Implicit in the term âexampleâ is the knowledge that the case is representative. You donât seem to be using the term in the accepted way.
You know, science doesnât work that way. If youâve got a hypothesis, you should make a significant effort to falsify it yourself before flaunting it in a forum.
You havenât shown anything that would suggest that such an overall pattern exists.
Good. So then it would seem that your claims about any overall pattern are at best premature, no?
Correlation is weak evidence for causation. Lack of correlation is very strong evidence against causation.
You havenât looked at any overall pattern. You have looked at perhaps three or four species. Several people have already pointed out that the bulk of the data on genome sizes do not fit the pattern you allege. Youâre the one looking at a few special cases, not the rest of us.
Itâs good to see you moderating your claims somewhat as you learn more about the subject, but then I have to wonder how on earth you felt confident enough to proudly proclaim that youâd come up with an overarching theory explaining genome sizes without having done the bare minimum amount of research? To not know about the famously massive lungfish genome? To have never heard of Paris japonica? These are among the very first species you hear about if you spend even 5 minutes googling on the subject.
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