This is part 11 of my review of The Myth of Junk DNA. For a list of other postings on this topic see the links in Genomes & Junk DNA in the "theme box" below or in the sidebar under "Themes." The title of Chapter 8 is "Some Recent Defenders of Junk DNA." It is Wells' attempt to deal with a very small percentage of the criticisms of his claim.
He begins with a reference to a 2003 paper that reported on transcription of a pseudogene and proposed a function for that transcript. He then references a 2006 paper that refutes the earlier study showing that the pseudogene transcript has no function. Good for Wells. That means he is aware of the fact that some of the work he references has not been reproduced. It's bizarre that Wells devotes three paragraphs to the discredited reference in Junk & Jonathan: Part 7—Chapter 4 and only mentions in passing that the result has been challenged.
He returns to this result in Chapter 8 and all but admits that the original result—so prominently presented in Chapter 3—is no longer valid. However, Wells can't leave it at that. The 2006 paper by Gray et al. went on to point out that some creationist literature had written up the earlier incorrect result and claimed that this was support for functional "junk DNA" and support for intelligent design creationism. The authors conclude their paper with ...
Furthermore, because Mkrn1-p1 is a nonfunctional pseudogene and does not trans-regulate its source Mkrn1 gene as claimed (6–9), our work reestablishes the evolutionary paradigm supported by overwhelming evidence that mammalian pseudogenes are indeed inactive gene relics.
This is too much for Jonathan Wells. He says, with apparently a straight face ....
Yet even if the results published by Gray and his colleagues were valid, their conclusion would not logically follow. Invalidating a report of one function in one pseudogene cannot exclude other possible functions in that pseudogene, much less possible functions in other pseudgoenes.Recall that this book quoted a dozen or so cases where a psuedogene might have a function in some species or another. This leads to the conclusion that all junk DNA is a myth. I wonder if Wells is irony deficient?
The sweeping pro-Darwin, anti-ID conclusion by Gray and his colleagues was obviously motivated by something other than evidence or logic—that is, by something other than science.Gray and his colleagues appear to motivated by some bizarre bias that Wells doesn't get. It's called truth.
The next example is the debate over pervasive transcription. I've already covered this in another posting [Pervasive Transcription].
Wells would like to believe that most of our genome is transcribed and this is evidence of function. Many scientists dispute the data, claiming that the appearance of pervasive transcription is an artifact. Others dispute the conclusion, claiming that the transcripts are merely junk RNA.
Wells tries to discredit some of the critics—especially the Toronto group—by bringing up technical details but he's in way over his head. The issue just can't be resolved as easily as Wells would like to believe. However, Wells reserves his harshest criticism for PZ Myers who had the audacity to blog about this last year [Junk DNA is still junk].
[PZ Myers] ... did not look at the methodology used by Hugh and his colleagues—a methodology guaranteeing that their results would appear to support the myth of junk DNA.In other words, Jonathan Wells has seen that the methodology of the Toronto group is so flawed that PZ Myers didn't recognize they were wrong. I'd put my money on PZ if I were you.
The Onion Test
The onion test is a simple reality check for anyone who thinks they have come up with a universal function for non-coding DNA1. Whatever your proposed function, ask yourself this question: Can I explain why an onion needs about five times more non-coding DNA for this function than a human?It's important keep in mind that this is a test that you should apply to any general explanation for junk DNA. For example, if you think that pervasive transcription means that almost all of the genome has a function then what kind of function requires five times as much in Allium cepa? And what kind of function requires five times as much DNA in A. ursinum compared to A. altyncolicum?
The onion, Allium cepa, is a diploid (2n = 16) plant with a haploid genome size of about 17 pg. Human, Homo sapiens, is a diploid (2n = 46) animal with a haploid genome size of about 3.5 pg. This comparison is chosen more or less arbitrarily (there are far bigger genomes than onion, and far smaller ones than human), but it makes the problem of universal function for non-coding DNA clear2.
Further, if you think perhaps onions are somehow special, consider that members of the genus Allium range in genome size from 7 pg to 31.5 pg. So why can A. altyncolicum make do with one fifth as much regulation, structural maintenance, protection against mutagens, or [insert preferred universal function] as A. ursinum?
So how does Wells handle this?
Biologist have long known that the DNA content (the "C-value") of eukaryotic cells varies by a factor of several thousand with no apparent correlation to organismal complexity or to the number of protein-encoding genes. There is a strong positive correlation, however, between the amount of DNA and the volume of a cell and its nucleus—which affects the rate of cell growth and division.Wells is implying that there's a cause-and-effect relationship between genome size and cell size. Presumably, the expansion of the genome was selected in order to increase cell size and slow down cell division. If that were true then why do different species of onion vary over a fivefold range in their genomic DNA content? And why does the common onion have five times more DNA that humans? Is it because onion plants grow much more slowly than humans?
Wells does not tell us why this correlation is important to his case and how it passes the onion test. Wells goes on to describe a correlation between metabolic rate and genome size in mammals and birds but he doesn't tell us how that relates to the idea that junk DNA is a myth. He also doesn't tell us what that correlation has to do with the Onion Test.
Theme
Genomes
& Junk DNA
... Gregory directs his challenge to "anyone who thinks they have come up with a universal function for non-coding DNA." Yet there probably is no such person. As we have seen, scientists know of many functions for non-protein-coding DNA. Nobody claims that there is "a universal function" that applies both to mammals and to onions.Nonsense! Several universal functions have been proposed: (1) that the huge amount of extra DNA is required for regulation; (2) that the extra DNA serves to protect the genes from harmful radiation; (3) the extra DNA is required for packaging chromatin; (4) the extra DNA is necessary to enhance recombination; (5) that large amounts of transposon DNA increases evolability; (6) large genomes make calls bigger; etc. etc.
When IDiots find it difficult to argue against good science they often shift the focus to something else. Wells likes this tactic and he uses it often.
Gregory misrepresents not only ID but also the logic of the argument. In 2007 he wrote. "It is commonly suggested by anti-evolutionists that recent discoveries of function in non-coding DNA support intelligent design and refute 'Darwinism.'" But Dawkins, Futuyma, Shermer, Collins, Kitcher, Miller, Coyne, and Avise argue exactly the opposite. They all claim that non-protein-coding DNA supports Darwinism and refutes intelligent design. It is their claim that is the issue here—and "recent discoveries of function in non-coding DNA" refute it. Gregory stands the argument on its head.There are two points here. Let's take them in reverse order.
So the onion test is a red herring. Why onion cells have five times as much DNA as human cells is an interesting question, but it poses no challenge to the growing evidence against the myth of junk DNA.
The Onion Test is meant to be a reality check for those who propose functions for junk DNA. In that sense, it poses a real challenge to those who advocate a function for junk DNA. Wells just doesn't get it.
The other point relates to the claim that evolutionary biologists point to the presence of junk DNA as proof of evolution. As a general rule, they do no such thing—although I won't be put in the position of defending every statement made by scientists. What evolutionary biologists often do is point to things like the comparison of pseudogene sequences in different lineages and explain how this is perfectly consistent with evolution by random genetic drift (but not Darwinism). They also point out that IDiots have never offered an explanation for the observed results of such comparisons. Why should known examples of junk DNA be found in the same locations in the genomes of related species?
Wells misunderstands arguments made by evolutionary biologists. He does this quite often. I think it's deliberate.
Gray, T.A., Wilson, A., Fortin, P.J., and Nicholls, R.D. (2006) The putatively functional Mkrn1-p1 pseudogene is neither expressed nor imprinted, nor does it regulate its source gene in trans. Proc. Natl. Acad. Sci. (USA) 103:12039-12044. [doi: 10.1073/pnas.0602216103]
Wells goes on to describe a correlation between metabolic rate and genome size in mammals and birds but he doesn't tell us how that relates to the idea that junk DNA is a myth.
ReplyDeleteOne really wonders how Wells would explain genome size reduction in birds. Following his kogic birds should be less complex than other tetrapods, In addition, if a higher metabolic rate would require higher complexities of the underlying apparatus how would Wells explain that newborns and children have a nuch higher metabolic rate compared to adults? BTW, I can actually significantly alter my metabolic rate without changing my genome size.
"Wells is implying that there's a cause-and-effect relationship between genome size and cell size. Presumably, the expansion of the genome was selected in order to increase cell size and slow down cell division. If that were true then why do different species of onion vary over a fivefold range in their genomic DNA content? And why does the common onion have five times more DNA that humans? Is it because onion plants grow much more slowly than humans?"
ReplyDeleteDo onion plants grow much more slowly than humans? How does one determine the answer to a question like that?
How does current evolution theory explain why an onion needs about five times more non-coding DNA than a human?
ReplyDeleteHow does current evolution theory explain why an onion needs about five times more non-coding DNA than a human?evolution theory doesn't say onions need more DNA than human and thus doesn't have to explain it.
ReplyDeleteHow does current evolution theory explain why an onion needs about five times more non-coding DNA than a human?
ReplyDeletethis should be a question for ID (there is no junk dna).
SPARC writes:
ReplyDeleteevolution theory doesn't say onions need more DNA than human and thus doesn't have to explain it.
To enlarge on that just a bit: The particular species of onion Gregory points to has through random mutation accumulated 5 times as much junk in its genome as humans. Other species of Allium have twice as much junk as that onion. The same theme (random variations in genome size - not variation in size in accordance with complexity) is demonstrated throughout life.
This is consistent with random variation, with selection retaining the relatively small proportion of critical genetic material. It is not consistent with intelligently directed design of genomes.
"To enlarge on that just a bit: The particular species of onion Gregory points to has through random mutation accumulated 5 times as much junk in its genome as humans. Other species of Allium have twice as much junk as that onion. The same theme (random variations in genome size - not variation in size in accordance with complexity) is demonstrated throughout life.
ReplyDeleteThis is consistent with random variation, with selection retaining the relatively small proportion of critical genetic material. It is not consistent with intelligently directed design of genomes."
But any adition of junk should be "selected" against the original DNA. Then junk should give an advantage and then it is not junk.
But worst for evolution is the "c paradox" How do you explain the diversity of DNA content in a common descent ramdom mutation and natural selection?
Blas writes:
ReplyDeleteBut any addition of junk should be "selected" against the original DNA.
The junk isn't selected. There's no reason to involve it in selection, since it's not important. It comes and goes at random.
Blas writes:
ReplyDeleteBut worst for evolution is the "c paradox"
Really? You think the existence of large amounts of junk DNA is a problem for evolutionary theory? You must not have read much literature on the subject for the past, oh, 40 years or so.
For theories of design, on the other hand, explaining why some intelligent entity would put a huge proportion of junk into its designs - now that's a problem.
@Jud For theories of design, on the other hand, explaining why some intelligent entity would put a huge proportion of junk into its designs - now that's a problem.
ReplyDeleteNot if you stick your fingers in your ears and jump up and down shouting "there is no junk DNA".
Evoution theory doesnt have to explain why the common onion has five times more DNA that human but evolution theory is the only way to explain how different genome sizes arose. In contrast to ID-creationism evolution theory is consistent with the molecular mechanisms that alter gene and genome sie (insertions, deletions, retrotransposition, transposition, chromosomal translocations etc.) and explains how such changes got fixed in populations through selection, drift and other mechanisms.
ReplyDeleteI took a quick look into the onion genomes and found:
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pubmed/18615255
Jakse et al 2008 Pilot sequencing of onion genomic DNA reveals fragments of transposable elements, low gene densities, and significant gene enrichment after methyl filtration.
Based on their initial sequencing screen, we can estimate that the onion genome is ~54% transposable elements (mainly inactive) compared to ~5% nuclear genes. Their discussion compares this to transposable element contributions to other genomes: 14% of rice, 50-60% of maize, and over 70% of barley genomes are made of transposable elements. My understanding is that the vast majority of junk DNA is composed of transposable elements, and that plants generally tend to accumulate it more than other organisms.
Previous posters indicate that they think this excessive load should be selected against. It's easy to think of a reason why it could be bad to carry useless DNA around in your genome: transposable elements can potentially disrupt coding genes, and every base pair needs precious phosphorous and nitrogen in order to be replicated before a cell can divide. Considering that there must be large tracts of genomic sequence that are both repetitive and non-adaptive, I imagine that unequal crossing over during meiosis could eliminate at least some of the junk DNA over time. The fact that this apparently hasn't happened (well, at least I think that is a safe assumption), then we should conclude that there is not enough selective pressure to eliminate the junk DNA, or in other words the junk DNA doesn't harm the organism enough to be selected against. So does it really make sense that these plants carry around so much junk?
I have a few thoughts on why it does make sense. The genomes we are looking at are all important crops for humans (that's why we sequenced them). I think this is relevant in a few ways. First, ancient humans probably decided to cultivate plants that were efficient at extracting key nutrients (ie: N and P) from the soil, for obvious reasons (ie: they are easier to cultivate than crops that require lots of fertilizer). Second, because these crops were being cultivated, they wouldn't have had to remain as competitive to survive, so even if transposable elements increased in the genome and subsequently made the crop plants less fit for surviving in the wild, it wouldn't have been selected against. Third, someone above mentioned that increased genome size is correlated with increased cell size. This is true with respect to polyploidy, but I'm not sure if it is true with respect to genomes with large compositions of junk DNA. If it is true for both, then losing large tracts of junk DNA during meiosis may have been selected against by human cultivators. Finally, and I'm really stretching it here, I imagine that having lots of junk DNA could potentially be adaptive for competition. Depleting nearby soil of as much P and N as possible could be adaptive in the sense that it reduces the amount of P and N available for nearby plants to use for their own growth. So if the plant is limited not by how much nutrient it can obtain, but rather by how much nutrient it can store, then transposable element increases would actually be beneficial and selected for.
I don't really want to start thinking about why the potentially negative impacts of transposable element insertions may not be bad enough to be selected against, since I've already written too much and chances are not many people are going to bother to read it, so I'll just say insertion bias.
Now let me predict a critical response of "just-so story". Well I agree, it is mostly hypothetical, but in principal all my ideas are testable. I'd welcome any thoughts on anything I wrote though.
"The junk isn't selected. There's no reason to involve it in selection, since it's not important. It comes and goes at random."
ReplyDeleteSo an onion carries 7 times the needed DNA only by chance!
That is a scientific answer!
I wonder if an onion that carries only 6,5 do not have an advantage. It means 8% less energy at each mitosis.
"Really? You think the existence of large amounts of junk DNA is a problem for evolutionary theory? You must not have read much literature on the subject for the past, oh, 40 years or so."
ReplyDeleteNo evolutionist explained how an homogeneus population of UCLA can evolve via RM+NS to the diversity of genomas sizes exist today.
No evolutionist explained how an homogeneus population of UCLA can evolve via RM+NS to the diversity of genomas sizes exist today.
ReplyDeleteA bit of a misunderstanding of the Last-Common-Ancestor concept. There is no reason to suppose that the population in which our LCA lived was homogeneous - it is merely the Last Ancestor Standing from those alive on the day it existed - all DNA in the world descends by template-mediated polymerisation from its DNA; descendants of all contemporary individuals are extinct. But no matter, genome doublings, polyploidy, LGT, hybridisation, transposable elements, endosymbiosis, meiotic misalignments (with a bias towards insertions, because deletions are more likely to be detrimental) provide more than adequate mechanisms to drive variation in DNA content between lineages descended from the LCA. I don't see how you get that no evolutionist can explain all this?
"all DNA in the world descends by template-mediated polymerisation from its DNA"
ReplyDeleteThis DNA was the smallest DNA possible or the biggest? RM+NS works by adding to a genoma or by substracting? How you get from the UCLA DNA by templated mediated polymerization to a protozoa that has 1000 more DNA than the average of protozoa? Carrying that quantity of junk give to this protozooa some advantage over his ancestors?
It seems to me there are three main possible explanations for the persistence of junk DNA:
ReplyDelete-junk DNA provides some advantage and accumulates because it is selected for.
-junk DNA is neutral and accumulates because it is not selected against.
-junk DNA is disadvantageous, but mechanisms that eliminate it from the genome are potentially more disadvantageous, so it accumulates faster than it can be eliminated.
Are there any other possible explanations? Any reasons why these explanations don't work?
"all DNA in the world descends by template-mediated polymerisation from its DNA"
ReplyDeleteThis DNA was the smallest DNA possible or the biggest?
Neither. It was as big as it was. Mechanisms exist both for adding and subtracting.
RM+NS works by adding to a genoma or by substracting? How you get from the UCLA DNA by templated mediated polymerization to a protozoa that has 1000 more DNA than the average of protozoa?
You need to be aware that there are a couple of very important transitions in that progression. The LCA was not a eukaryote ("protozoon"). Prokaryotes (in which we can assume LCA to be placed) are selected for very economical genomes. They are limited by replication, so their genomes don't grow much. Eukaryotes formed from endosymbiosis between two prokaryotes - there have been other endosymbiotic events too. This adds DNA. They also discovered sex (meiosis). It's this that really muddies the waters, both because of meiotic misalignment and the role of 'selfish DNA'. Many genetic elements are actually sexually transmitted 'diseases'. Eukaryotes are NOT limited (as much) by replication costs. Their genomes are thousands of times bigger than bacteria. But because they have mitochondria and more efficient feeding and locomotor systems, their income better covers their expenditure. So they can carry a lot more crap around without being unduly inconvenienced by it. Variation within eukaryotes is not forbidden. You seem to think that evolution demands that all change be beneficial, and what happens in one organism must also happen in another. It doesn't.
Carrying that quantity of junk give to this protozooa some advantage over his ancestors
No. You don't need any advantage over your ancestors; they are dead.
"Are there any other possible explanations? Any reasons why these explanations don't work?"
ReplyDelete1) Then it is not "Junk"
2)and 3) Needs an explanation why carying so much DNA is neutral or less expensive than eliminate it.
"No. You don't need any advantage over your ancestors; they are dead."
ReplyDeleteNo, you have the "evolved" specimen in the middle of the population from it "evolved". Then the offsprings of the onion with biggest genoma prevailed over the offsprings of the original onions. That is what ToE explains about how both species of onions should be formed from their common ancestor.
Blas writes:
ReplyDeleteSo an onion carries 7 times the needed DNA only by chance!
That is a scientific answer!
What on Earth makes you think random chance is "unscientific" as a factor in genome size?
Do you not think chance plays a role in success, failure and change of species? Or do you think the Designer was really, really pissed off at dinosaurs, so he turned them into chickens, like some angry wizard in a children's fairy tale?
"No. You don't need any advantage over your ancestors; they are dead."
ReplyDeleteNo, you have the "evolved" specimen in the middle of the population from it "evolved".
Individuals don't evolve; populations and lineages do.
Then the offsprings of the onion with biggest genoma prevailed over the offsprings of the original onions. That is what ToE explains about how both species of onions should be formed from their common ancestor.
Nope. When you are considering the relative performance of two species with different genome sizes, you have to remember that species form by some isolating mechanism that prevents genes spreading between two populations. Nothing that happens in A constrains anything that happens in B - they are each free to drift in a direction that might be selectively eliminated if the populations mixed freely.
Let's forget about onions. Let's just think about a generic organism with a genome size of x. The whole population has the same size genome. An error in meiosis gives a genome size of x+y to one individual. If that is to be selected against, and eliminated from the population, it must have a negative effect on survival or reproduction. You are free to make up a critical value of y that allows the change to slip 'under the radar' and not be selected against. 1 extra base? 100? 1000? 10,000? You can stick the value where you like, but as long as it is not zero, the genome can grow by that amount without reducing fitness against other members of the population that have stuck with x.
This mutation can spread through the population by genetic drift - there is no force opposing it. Then, the whole population has a genome size x+y. We're back where we started, but with a bigger genome. Then a mutation occurs that generates a genome of size x+y+z ...
You might expect a balancing move in the opposite direction - a genome of x-y could also spread. But in this case, there is a likelihood that removal of y will cause damage by removing a 'real' gene. So x+y tends to be more likely to survive than x-y. You get a ratchet. I think you'd be surprised at how much genome expansion can be tolerated with no apparent fitness effects, even without invoking ratcheting. Whole genome doublings are common.
Of course, this bloating cannot proceed indefinitely. But it can proceed a long way.
Allan Miller writes:
ReplyDeleteAn error in meiosis gives a genome size of x+y to one individual.
Or, as long as we're speaking of junk and common sources thereof, a retrovirus is integrated into the genome as a retrotransposon.
Blas said...
ReplyDelete"Are there any other possible explanations? Any reasons why these explanations don't work?"
1) Then it is not "Junk"
2)and 3) Needs an explanation why carying so much DNA is neutral or less expensive than eliminate it."
That sounds right. I wonder if people here will respond to you.
Blas may not be aware that it is quite likely that he is carrying significantly more or less DNA than his nearest relatives: Redon et al. (doi:10.1038/nature05329)identified "a total of 1,447 copy number variable regions (CNVRs), which can encompass overlapping or adjacent gains or losses, covering 360 megabases (12% of the genome) in human populations.
ReplyDelete2)and 3) Needs an explanation why carying so much DNA is neutral or less expensive than eliminate it."
ReplyDeleteStart by reading Orgel and Crick 1980. Don't come back until you understand it. No, I won't do the work for you.
Jud,
ReplyDeleteOr, as long as we're speaking of junk and common sources thereof, a retrovirus is integrated into the genome as a retrotransposon.
Indeeed - I listed a number of possible sources of DNA addition in an earlier reply, but thought I'd just pick an endogenous source for the breakdown.
Transposons, and sexual transmission thereof, are likely a prime source of divergence, since each 'infection' is a standalone event. And they can drive against a gradient of fitness depression; they don't necessarily need drift (although that depression is more likely to come from mutagenesis than genome size expansion per se). Once the whole population is infected, they are all back to being equally fit wrt genome size.
I think people overestimate how much it costs a well-fed eukaryote to replicate surplus DNA. I carry about 180 pounds of material that is clearly not essential for survival as a genome, even if it is necessary for this genome.
"Wells is implying that there's a cause-and-effect relationship between genome size and cell size. Presumably, the expansion of the genome was selected in order to increase cell size and slow down cell division. If that were true then why do different species of onion vary over a fivefold range in their genomic DNA content? And why does the common onion have five times more DNA that humans? Is it because onion plants grow much more slowly than humans?"
ReplyDeleteDo onion plants grow much more slowly than humans? How does one determine the answer to a question like that?
Yes I suppose advantageous DNA isn't junk.
ReplyDeleteIt shouldn't be hard to imagine a situation where junk DNA is neutral. If the growth/survival to reproductive age of an organism is not limited by DNA replication, then individuals with additional DNA would not be any worse off, and additional DNA could be fixed in the population by genetic drift. The fact that transposable elements replicate themselves means that genomes would increase in size over time. Eventually genome size approaches a point where replication is limiting, and there would be some advantage to having a lower amount of junk DNA. But at any given time in a population, there probably isn't a huge difference in the amount of junk DNA each individual is carrying. There probably won't ever be strong selection for individuals with less junk DNA, unless part of the population acquires a new transposable element that is accumulating copies of itself over several generations, creating a significant selectable difference between individuals.
The problem with eliminating junk is that I can't think of any mechanisms for an organism to specifically remove junk DNA from its genome (although there are mechanisms for reducing the activity of self replicating junk). It is probably limited to mechanisms like unequal crossing over to cause deletions and remove junk DNA. If an organism would be better off with less junk DNA, I suppose we might think that mutations which increased the frequency of unequal crossing over would become advantageous.
But there are problems here to address. First, unequal crossing over results in a deletion on one homologous chromosome, and a duplication on the other homologous chromosome. So any given offspring of any genotype is just as likely to have an increase or decrease in junk DNA due to unequal crossing over. Second, unequal crossing over can potentially result in a deletion/duplication of functional DNA, which would generally not be advantageous. So, a mutant allele that increases the frequency of unequal crossing over should only persist in a population if the benefit of additional junk deletions in some offspring outweighs the disadvantage of additional junk duplications plus additional duplications/deletions of functional DNA. So perhaps there is some positive relationship between the amount of junk DNA and the rate of unequal crossing over, but it is not clear to me how this would be sufficient to bring the amount of junk DNA below the threshold where it stops having a negative impact on the organism.
The best strategy for dealing with transposable element junk seems to be supressing their activity rather than eliminating them outright.
"Blas may not be aware that it is quite likely that he is carrying significantly more or less DNA than his nearest relatives: Redon et al. (doi:10.1038/nature05329)identified "a total of 1,447 copy number variable regions (CNVRs), which can encompass overlapping or adjacent gains or losses, covering 360 megabases (12% of the genome) in human populations."
ReplyDeleteFirst: We are talking of 7 times the genome in the case of the onions, the differences may be even worst 1000 times difference, the scale of the C´value is logaritmic.
Second: So Toe predicts that the genomes constantly growths?
" Allan Miller said...
ReplyDeleteOf course, this bloating cannot proceed indefinitely. But it can proceed a long way."
But the result of an ramdom process like this should be a distribution genomes sizes strating with a minimun and being asintotic to a maximum, and following the "age" of the genome.
" Negative Entropy said...
ReplyDelete2)and 3) Needs an explanation why carying so much DNA is neutral or less expensive than eliminate it."
Start by reading Orgel and Crick 1980. Don't come back until you understand it. No, I won't do the work for you."
They explain how we get more DNA,not why that is selected or why some species have more and another less. And we are talking about 10, 100, 1000 times not the double.
" Allan Miller said...
ReplyDeleteOf course, this bloating cannot proceed indefinitely. But it can proceed a long way."
But the result of an ramdom process like this should be a distribution genomes sizes strating with a minimun and being asintotic to a maximum, and following the "age" of the genome.
Totally incorrect, I'm afraid. The result of a random process in mathematics produces a probability distribution of some kind. It is not the shape of the distribution, but the existence of it, that distinguishes a random process. A roulette wheel with a strong magnet under one of the numbers will produce a probability distribution, and spins would be random even if biased.
But the answer to your conundrum is hinted at in my long post - I can't expect you to have read it all, of course, so I will spell it out.
When a genome is fully packed with valuable genes - to paraphrase Monty Python, "every base is sacred" - then mutations of the type "x-y" - removing bases - will all be lethal. Therefore, although x+y and x-y may occur with equal frequency, only x+y mutations will survive. By progressive bloating, biased in an upward direction by greater lethality for x-y, junk increases.
As junk is added, we find that x-y mutations are lethal less and less frequently, because the "y" bases that are removed are increasingly likely to be dispensible junk. Therefore, the upward growth is counterbalanced by increase in the rate of base removal, and does not continue indefinitely.
You are also wrong because you think I offered an expectation of linearity with "genome age". All genomes are the same age, in time since common ancestry. But each species has a different history, in the bases added and subtracted, the role of transposon infestation and massive chromosomal duplications since common ancestry. There is no apparent constraint insisting that genomes should follow any kind of pattern in terms of their size or their packing, as borne out by extensive within-genus variation. It's not evolution that expects perfectionism in every organismal character!
"Wells is implying that there's a cause-and-effect relationship between genome size and cell size. Presumably, the expansion of the genome was selected in order to increase cell size and slow down cell division. If that were true then why do different species of onion vary over a fivefold range in their genomic DNA content? And why does the common onion have five times more DNA that humans? Is it because onion plants grow much more slowly than humans?"
ReplyDeleteDo onion plants grow much more slowly than humans? How does one determine the answer to a question like that?
Since nobody has answered this question I conclude that indeed onions do grow much more slowly than humans.
In that case the onion is no longer a problem.
Since nobody has answered this question I conclude that indeed onions do grow much more slowly than humans.
ReplyDeleteIn that case the onion is no longer a problem.
Tumbleweed ... tolling bell ...
Yes, the world of science is indeed stunned into silence by this amazing piece of comparative biology.
By comparing two species that have virtually no commonality in their developmental mechanisms and requirements, and evolved multicellularity completely independently, we see the Designer's plan laid bare. Because of course c-value is the sole determinant of growth rate ... isn't it?
http://www.youtube.com/watch?v=79XDphLskCY
My kids grew like that, from a point at the top of their heads.
Allan Miller writes:
ReplyDeleteMy kids grew like that, from a point at the top of their heads.
Ah, perhaps you haven't heard the old Yiddish insult:
Soll's wachsen wie ein Tzibbele, mit dem Kopf in Drerd!"
("You should grow like an onion, with your head in the ground!")
If there is virtually no commonality in onion and human developmental mechanisms and requirements, and they evolved multicellularity completely independently,
ReplyDeletethen why are onions considered a problem?
"As junk is added, we find that x-y mutations are lethal less and less frequently, because the "y" bases that are removed are increasingly likely to be dispensible junk. Therefore, the upward growth is counterbalanced by increase in the rate of base removal, and does not continue indefinitely."
ReplyDeleteNice story but do not explain why one onion growth 7 times more the other, or why birds have a genoma smaller than the average of reptiles.
"Since nobody has answered this question I conclude that indeed onions do grow much more slowly than humans."
ReplyDeleteA mind capable of reaching strong logical conclusions such as this couldn't possibly have evolved by random collisions of atoms. Ok I'm a creationist now.
rez_imotoboleht may be on to something.
ReplyDeleteBut I am not a "creationist".
@Jud
ReplyDeleteMy kids grew like that, from a point at the top of their heads.
[...]
"You should grow like an onion, with your head in the ground!"
I thought something was going wrong developmentally when they were just chives! :0)
"As junk is added, we find that x-y mutations are lethal less and less frequently, because the "y" bases that are removed are increasingly likely to be dispensible junk. Therefore, the upward growth is counterbalanced by increase in the rate of base removal, and does not continue indefinitely."
ReplyDeleteNice story but do not explain why one onion growth 7 times more the other, or why birds have a genoma smaller than the average of reptiles.
OK, I'm going to give in to the temptation to lose my temper now. I know this is just what you want, and you an your many mates Anon can crow about those beastly evolutionists, but that is just f***ing MORONIC.
I have patiently explained the general principles underlying genome expansion/contraction, and you have not understood one frigging word!
Why does your precious designer make one onion "growth" 7 times more than the other? Or why birds have a "genoma" smaller than the average of reptiles? I confidently predict that you haven't a f***ing clue. But you are certain that, whatever the reason, it must be a damn good one, 'cos it's the Creator and stuff.
So when I explain that the reason may lay in the essential neutrality of genome expansion, and upward bias, and variation due to essentially stochastic factors, and that point goes whooshing over your head so you ask the "perfectionist" question again - "OK Mr smarty pants evolutionist, why is THIS organism like it is?"
[...] deep breath [...]
Then I give up. Education is a 2-way street; the consumer has to be incentivised by a desire to understand (or at least to pass an exam). But you revel in your 10-minute-biology level of understanding, which gives you enough education to take on all those professors and degree-holders. You win, good troll, all hail the Creator of Onions genomically great and small.
It's a good job I write for my own amusement!
@Anon
ReplyDeleteIf there is virtually no commonality in onion and human developmental mechanisms and requirements, and they evolved multicellularity completely independently,
then why are onions considered a problem?
Because multicellularity is not the issue. Nor is development or growth. The challenge is to pick a function and determine why an onion needs about five times more non-coding DNA for this function than a human.
You could try growth or differentiation, but I'd just laugh at you. Try again.
You could also explain Blas's seven-fold difference within the onion family, if you prefer something a bit more closely related.
Here's a hint: don't get too hung up on the multicellular thing. Biosynthetic and catabolic pathways, the machinery of error repair, mitosis and meiosis, mitochondrion farming, protein synthesis and so on - these are the central processes for onion and human, not the bulding of large somatic structures.
You could look at chloroplast farming, or vacuolisation, or cell wall construction ...
I just googled "Onion Test", and the top result was:
ReplyDelete"In The Know: Are Tests Biased Against Students Who Don't Give A Shit?" from ... The Onion!
:0)
Damn, looks like I missed out on some fun threads I could have totally contributed to while in the midst of moving-related upheaval...
ReplyDelete