The total size of the human genome is estimated to be 3.2 × 109 bp [How Big Is the Human Genome?]. Here are the major components.
Transposable Elements: (44% junk)
DNA transposons:
- active (functional): <0.1%
- defective (nonfunctional): 3%
- active (functional):<0.1%
- defective transposons (full-length, nonfunctional): 8% L1 LINES (fragments, nonfunctional): 16% other LINES: 4% SINES (small pseudogene fragments): 13%
- co-opted transposons/fragments: <0.1% a
aCo-opted transposons and transposon fragments are those that have secondarily acquired a new function.
- active (functional): <0.1%
- defective DNA viruses: ~1%
- active (functional): <0.1%
- defective (nonfunctional): 8%
- co-opted RNA viruses: <0.1% b
bCo-opted RNA viruses are defective integrated virus genomes that have secondarily acquired a new function.
- (from protein-encoding genes): 1.2% junk
- co-opted pseudogenes: <0.1% c
cCo-opted pseudogenes are formerly defective pseudogenes those that have secondarily acquired a new function.
- essential 0.22%
- junk 0.19%
- tRNA genes: <0.1% (essential)
- known small RNA genes: <0.1% (essential)
- putative regulatory RNAs: ~2% (essential)
- transcribed region:
essential 1.8% intron junk (not included above) 9.6% ddIntrons sequences account for about 30% of the genome. Most of these sequences qualify as junk but they are littered with defective transposable elements that are already included in the calculation of junk DNA.
- essential 0.6%
- <0.1% (essential)
- <0.1% (essential)
- α-satellite DNA (centromeres)
- essential 1.0%
- non-essential 2.0%
- telomeres
- essential (less than 1000 kb, insignificant)
- conserved 2% (essential)
- non-conserved 26.3% (unknown but probably junk)
For references and further information click on the "Genomes & Junk DNA" link in the boxLAST UPDATES: May 10, 2011 (fixed totals, and ribosomal RNA calculations) June 3, 2011 (added total genome size) February 5, 2013 (reformatted)
This is brilliant - we'll be posting about it on Genome Engineering http://www.genome-engineering.com/whats-in-your-genome.html
ReplyDeleteNice summary! I'll use it in my genetics course.
ReplyDeleteThis conforms to my general impression but I would like to see reference(s) for the specific numbers. E.g., functional vs defective RNA viruses.
ReplyDeleteDK asks,
ReplyDeleteThis conforms to my general impression but I would like to see reference(s) for the specific numbers. E.g., functional vs defective RNA viruses.
Good question! I haven't yet posted a specific description of the Human Endogenous Retroviruses (HERVs). Check out Kurth and Bannert (2010) [Int J Cancer 126:306-314] for a review of the subject.
The only functional retroviruses in the human genome are the ones belonging to the HERV-K class. All the others have multiple mutations that make then defective. There appear to be about 100 recent sites of HERV-K insertion but most of the retroviruses at these sites have mutations. Site HERV-K113 is almost certainly functional but it seems like there may only be a few more in the human genome.
That's the basis of my estimate that <1% of the endogenous retrovisuses are active.
Do you have any reason to doubt this number?
Do you have any reason to doubt this number?
ReplyDeleteNot, not really. I asked for my own education only. I know very few hard facts about viruses in genomes.
With the multitude of human viruses, I would have thought that over time most of them managed integration into a germline. At least weaker versions of them that don't mess up cells too much should then just stay there. So I expected more than just retroviruses and more than ~10% of active viruses.
Thanks for this - fascinating.
ReplyDeleteI have one question - how do you get to 8.5% being essential - is this different from being functional?
To replicate this 8.5% figure I've had to exclude all amounts which are quantified as being < 1%.
If I assume that it is possible to say <1% means at most 1% (or whatever) for these figures (seems reasonable!) - then it would seem to put functional/essential elements discovered so far to be no more than about 16% - ie nearly double the figure you've given.
With your total adding up to 98% I assume you are hedging your bets, which is totally understandable given the state of the science, but the lacunas this creates are a bit of a confusion.
Regards.
I'm going to quibble with your assessment of the rRNA genes and the false dichotomy between 'essential' and 'junk' in this specific case. While only 1/3 may be actively used to generate rRNA in a mitotic cell, all of the rRNA genes are 'functional' in the sense that in the germline having abundant numbers of nearly sequence-identical genes in high local concentration keeps the non-allelic meiotic recombination rate in the rDNA high, thereby preserving the homogeneity of the rDNA sequences. Trimming off the 'extra' copies of rDNA genes will reduce the rate of gene conversion in the rDNA compromising the evolutionary capacity of the rDNA to maintain functional primary sequence. The relative importance of this phenomenon for a functional human genome is unclear, but since S. cerevisiae uses a similar rDNA genomic architecture strategy, it is reasonable to hypothesize that the 'extra' copies are in fact relevant to the success of the species population, keeping in mind that evolution is a population-based phenomenon rather than a single organism phenomenon.
ReplyDelete@Chinahand,
ReplyDeleteIf I assume that it is possible to say <1% means at most 1% (or whatever) for these figures (seems reasonable!) - then it would seem to put functional/essential elements discovered so far to be no more than about 16% - ie nearly double the figure you've given.
Thanks for pointing this out. When I said <1% I meant WAY less than 1% but I can see how that might have been confusing. I've fixed all those numbers to read "<0.1%"—hope this helps.
I've also adjusted the "unknown" value to 26.5% so everything adds up to 100%.
Thanks again.
Andy Pierce says,
ReplyDeleteI'm going to quibble with your assessment of the rRNA genes and the false dichotomy between 'essential' and 'junk' in this specific case.
I explained the organization of ribosomal RNA genes in: Human Ribosomal RNA Genes.
The 5S RNA genes are arranged as a single tandem cluster on chromosome 1 (1q42). The repeats are 2.2 kb but the gene itself is only 200 bp. The number of repeats varies from individual in the range of 35-175 copies. I estimate that the average size of the cluster is 220 kb and more than half of the repeat could be deleted without any effect. (The length of the repeat varies from species to species.
The 18S/5.8S/28S/ ribosomal RNA genes are found in five different clusters as 43 kb repeats. Most of this repeat is non-transcribed spacer and I estimate that a lot of it is non-essential DNA that could easily be deleted without any effect on the individual or the species. (The length of non-transcribed spacer varies from species to species.)
I agree with you that even the ribosomal psedugoenes may be required in the long run. That's why I ended the posting with ...
The minimum number of 45S genes in mammals is not known for certain in humans but in chickens the loss of anything more than half the average number is lethal. It seems reasonable that of the 300 or so human 45S genes only about 150 are absolutely required and the remainder are dispensable. However, concerted evolution of these genes is essential in the long run and the mechanism of concerted evolution and gene conversion requires lots of copies. Thus, all copies are necessary for the species even though only half may be required for any one individual.
Thanks for alerting me to a problem with the calculations. I've fixed the numbers.
The minimum number of 45S genes in mammals is not known for certain in humans but in chickens the loss of anything more than half the average number is lethal.
ReplyDeleteThe chicken data on rDNA copy number notwithstanding, the effect of rDNA insufficiency in humans is unknown. Clearly a severe insufficiency will be lethal, but there is unlikely to be a sharp demarcation between 'enough = totally fine' and 'not enough = dead'. For this reason, the division of rDNA gene content into 'essential' and 'junk' is an oversimplification. I hypothesized that non-lethal human rDNA insufficiency would manifest in humans as Diamond-Blackfan anemia of variable clinical severity determined by the level of rDNA insufficiency, drawing parallels to the way in which DBA is known to be caused by ribosomal protein insufficiency, but unfortunately, the NIH declined to fund these studies.
In terms of the effects of the length of the non-transcribed spacer on the efficiency of rDNA gene conversion and architectural rearrangement, much will depend upon the efficiency of meiotic recombination with respect to the interplay of multifactorial considerations including unit repeat length, repeat copy number, total number of gene clusters, and sub-nuclear multi-cluster organization (such as nucleolar co-localization). This area of meiotic biology is very poorly understood.
I like your revised estimate that over half of the rDNA is essential, but the rest is going to be progressively less essential. The point at which 'less essential' slides over into 'junk' is a judgement call.
Andy Pierce says,
ReplyDeleteThe chicken data on rDNA copy number notwithstanding, the effect of rDNA insufficiency in humans is unknown.
Right. That's why I said that every single gene is essential if we assume an average of 300 45S genes per genome. There's no junk in those genes even though some of them are pseudogenes.
I like your revised estimate that over half of the rDNA is essential, but the rest is going to be progressively less essential. The point at which 'less essential' slides over into 'junk' is a judgement call.
Of course it's a judgment call. I'm assuming that a large part of the spacer DNA is junk because there are plenty of species that have much shorter spacers.
If you have a better estimate that you prefer then please let me know. Remember we're quibbling over something like 0.1% of the genome. Do you think that's an important point? Why?
Remember we're quibbling over something like 0.1% of the genome. Do you think that's an important point? Why?
ReplyDeleteNo, the important point is that for some aspects of the genome, like the rDNA, the strict binary classification of "essential" vs "junk" is inaccurate because it excludes the potential for a lot of middle ground between "can't live without it" and "of no use whatsoever". There needs to be a third category along of the lines of "confers a fitness advantage under some circumstances", or whatever you'd prefer to call it.
The relevance of the lengths of the spacers in other species is hard to assess due to species-specific differences in recombination efficiency determinants, many of which are understood poorly or not at all, particularly in the meiotic context.
Man, this post seems to have really shut up the crazies. Where are the posts from the IDiots, the doubters, the creationists, et al...?
ReplyDeleteAndy Pierce says,
ReplyDeleteNo, the important point is that for some aspects of the genome, like the rDNA, the strict binary classification of "essential" vs "junk" is inaccurate because it excludes the potential for a lot of middle ground between "can't live without it" and "of no use whatsoever". There needs to be a third category along of the lines of "confers a fitness advantage under some circumstances", or whatever you'd prefer to call it.
That category is already covered under "essential" and "functional." I would never classify such a sequence as "junk."
anonymous asks,
ReplyDeleteMan, this post seems to have really shut up the crazies. Where are the posts from the IDiots, the doubters, the creationists, et al...?
Not to worry. I'm sure they are busy researching the question and they'll post a detailed explanation of why all that junk DNA is actually functional.
Watch for it on the creationist web sites. Any day now ....
Where are the posts from the IDiots, the doubters, the creationists, et al...?
ReplyDeleteI think it's all the numbers, it's got them confused. Probably using them to look up verses in the bable.
You've been told *over and over* again, Larry, that just because you don't know the exact function of something doesn't make it junk.
ReplyDeleteThis is an argument from ignorance.
Much of the genome may be "non-essential" but this does not make it evolutionary garbage.
4% of the universe is matter as we know it, with the rest either dark matter or dark energy (according to theoretical cosmologists).
I strongly believe that intergenic ncDNA helps maintain structural stability and also shields coding DNA from harmful mutations and viruses.
The packaging is sometimes as important as the present itself. If you don't wrap it up well, then you could end up causing damage to the gift.
Atheistoclast says,
ReplyDeleteYou've been told *over and over* again, Larry, that just because you don't know the exact function of something doesn't make it junk.
Thanks for reminding me. I agree with you, in principle.
However, when we know that 44% of our genome consists of defective transposons we can be pretty sure that they are junk.
Would you like to argue that it's more likely that all these defective transposons have a secret unknown function that has remained hidden for four decades?
Go for it.
You've been told over and over again that there are sound logical reasons for assuming that most of our genome is junk. It's not an argument from ignorance.
The argument from ignorance comes from those people who don't understand the topic. This posting was designed to remedy that situation.
There is a wealth of evidence that repetitive DNA (including retrotransposons) do play an important part in stabilizing the DNA molecule in eukaryotes (see research on the GC content) .Also, it need not have an "active" function. I suspect introns, for example, mostly serve as spacer sequences to facilitate alternative splicing etc.
ReplyDeleteAll the same, LTR elements do serve to modulate gene expression, even at a distance. The mechanism is still poorly understood. They are hardly defective. Why has natural selection conserved all this "junk DNA"? Why are 70-90% of plant genomes made of the stuff? To accumulate all this "garbage" would impose to high of a metabolic cost on the organism.
I think you are arguing that the core information content of the genome is about 9% - agreed. But that doesn't mean the rest is useless.
Atheistoclast:
ReplyDeleteI strongly believe that intergenic ncDNA helps maintain structural stability and also shields coding DNA from harmful mutations and viruses.
Belief (per se) has no currency in science. Do you have any substantial evidence for this claim?
If you're suggesting that the junk DNA hypothesis itself is an argument from ignorance, then the ignorance is yours. There's lots of supporting data; just read Dr. Moran's posts, fercrissake! If you want to dispute that evidence or offer contrary evidence, great! Please do. Otherwise, there's no reason to take you seriously.
Atheistoclast says,
ReplyDeleteThere is a wealth of evidence that repetitive DNA (including retrotransposons) do play an important part in stabilizing the DNA molecule in eukaryotes (see research on the GC content).
I'm not aware of this "wealth" of evidence. Could you post one or two references?
I suspect introns, for example, mostly serve as spacer sequences to facilitate alternative splicing etc.
I'm not saying that all intron sequences are junk. I'm saying that based on the variation we seen within a population and between closely related species, the majority of intron sequences are dispensable junk.
I doubt that large intron sequences are needed to facilitate alternative splicing since only a small percentage of human genes exhibit biologically functional alternative splicing.
All the same, LTR elements do serve to modulate gene expression, even at a distance.
Please supply references to the scientific literature showing that a significant percentage of LTR's play a biologically relevant role in modulating gene expression. I'm not denying that there are half a dozen examples but that amount is insignificant in the grand scheme of things.
Why has natural selection conserved all this "junk DNA"?
It hasn't. Get your facts straight.
To accumulate all this "garbage" would impose to high of a metabolic cost on the organism.
Have you ever heard of the C-Value Paradox or The Onion Test? The scientific evidence shows pretty conclusively that the presumed cost is insignificant for most species.
I strongly believe that intergenic ncDNA helps maintain structural stability and also shields coding DNA from harmful mutations and viruses.
Perhaps you like to explain how junk DNA could shield coding DNA from mutations and viruses? Here's something you might like to read before answering: Does Excess Genomic DNA Protect Against Mutation?. I suspect you haven't though about this very deeply.
Perhpas you'd like to explain how junk DNA could help maintain structural stability? Do species with much less junk DNA have unstable genomes? Some species of frog have 100X more DNA than closely related species. Is that because their genome is extremely stable?
Larry,
ReplyDeleteIntrons affect the stability of the mRNA transcript. I quote from this paper:
Introns and mRNA stability
By analyzing the genome-wide data of mRNA stability published by someone previously, we found that human intron-containing genes have more stable mRNAs than intronless genes, and the Arabidopsis thaliana genes with the most unstable mRNAs have fewer introns than other genes in the genome.
They also affect gene expression in subtle ways. You have blue eyes in part because of a mutation in an intron causing a reduction in melanin concentration in your iris:
Introns work in mysterious ways
The point about LTRs is that they can modulate gene expression - even you accept this. if many are inactive/defective right now,they could be later on - and selection will favor those individuals who have the most preserved sequences.
The problem with you is that you are a deep thinker who is not thinking across deep time. You are just looking at the genome and seeing no current potentiality in vast swathes of it when there exists the possibility of future uses and effects.
There is no doubt that ncDNA can shield exonic regions from any harmful retroviral insertions or from illegitimate recombination. I was not referring to point mutations.
As for frogs, I am not sure - 100x sounds excessive. Salamanders also have enormous genomes. If I were a researcher I would investigate possible reasons for a relationship rather than just dissing it.
@Atheistoclast,
ReplyDeleteIs that all you've got?
You base your skepticism about junk in introns on papers like that?
The problem with you is that you are a deep thinker who is not thinking across deep time. You are just looking at the genome and seeing no current potentiality in vast swathes of it when there exists the possibility of future uses and effects.
As I deep thinker I know a thing or two about evolution. The fact that sometime in the next million years there might be a small piece of junk DNA that evolves a new function is no reason to dismiss the evidence that most of our genome is junk. And in case you think otherwise, let me assure you that there cannot be SELECTION for potential future uses. Evolution doesn't work that way.
There is no doubt that ncDNA can shield exonic regions from any harmful retroviral insertions or from illegitimate recombination. I was not referring to point mutations.
How, exactly, does that work? The more junk DNA you have the bigger the target for retrovirus insertions that will cause no harm. Hence, those species with large genomes (i.e. us) carry a lot of retroviruses.
In species with small genomes the average insertion will be lethal and quickly weeded out of the population.
Do you think there's an adaptive reason to provide a bigger target for retroviral insertions?
As for frogs, I am not sure - 100x sounds excessive. Salamanders also have enormous genomes. If I were a researcher I would investigate possible reasons for a relationship rather than just dissing it.
Investigations have been underway for at least forty years. Don't you think it's time we started to entertain the idea that there may not be a reason why closely related species have vastly different amounts of DNA?
Why do I get the feeling that all this is new to you?
"
ReplyDeleteAnd in case you think otherwise, let me assure you that there cannot be SELECTION for potential future uses.
"
Just to play Devil's Advocate, you can completely inactivate telomerase in mice with no appreciable phenotype until the mice have been bred for 6 or 7 generations. Why doesn't this count as selection for potential future use?
Larry,
ReplyDeleteBoth introns and UTRs play an important part in molecular stability. That is increasingly obvious. Their utility is subtle.
Let me assure you that there cannot be SELECTION for potential future uses. Evolution doesn't work that way.
No, you don't seem to understand how selection can have a long reach into the future - I am very disappointed. Here is an example:
If element A is useless now but turns out to be useful later on, then those individuals with the most preserved (functioning) element As in their genomes will feel its beneficial effects compared to those with defective and degenerate ones. As such, they will become more prevalent because of differential reproduction. OK?
In species with small genomes the average insertion will be lethal and quickly weeded out of the population.
That is precisely the point. Both ncDNA, and also duplicate protein-coding genes, serve as buffers against harmful effects in the *individual* organism. In fact, I can see how both the accumulation of duplicate genes (80% of eukaryotic genes are paralogs of others) and ncDNA might set off evolutionary arms races. It is a case of must having something only because someone else does - the actual net benefit needs not exist.
Now, the reason why I mentioned "illegitimate recombination" is because uni-chromosomal prokaryotes don't recombine their DNA as eukaryotes do. Since illegal recombinatory events can cause frameshifts in coding DNA, ncDNA (especially intergenic sequences) serves as a protective shield against them.
Don't you think it's time we started to entertain the idea that there may not be a reason why closely related species have vastly different amounts of DNA?
I would be more interested in why amphibians have so much ncDNA compared to others. I know you think of this as coincidence and accidence but I think that is a lazy answer. Also, 40 years ago we didn't have the genomic analysis tools we have now. It is a brave new world you want to destroy, Larry.
Atheistoclast writes:
ReplyDeleteIt is a brave new world you want to destroy, Larry.
How unintentionally appropriate. Consider this excerpt from The Tempest, from which the phrase "brave new world" comes:
MIRANDA: ...O brave new world,
That has such people in't!
PROSPERO
'Tis new to thee.
...and compare that to Larry's comment on a previous posting of yours:
Atheistoclast: If I were a researcher I would investigate possible reasons for a relationship rather than just dissing it.
Larry: Investigations have been underway for at least forty years.... Why do I get the feeling that all this is new to you?
Atheistoclast writes:
ReplyDeleteIn fact, I can see how both the accumulation of duplicate genes (80% of eukaryotic genes are paralogs of others) and ncDNA might set off evolutionary arms races. It is a case of must having something only because someone else does - the actual net benefit needs not exist.
What unmitigated junk, pun fully intended. I must have something with no benefit (or deleterious) because someone else does, and that leads to an "arms race"? So if my neighbor is in hock up to his eyeballs, I better accumulate massive debt as well or be left behind?
@Atheistoclast If element A is useless now but turns out to be useful later on, then those individuals with the most preserved (functioning) element As in their genomes will feel its beneficial effects compared to those with defective and degenerate ones. As such, they will become more prevalent because of differential reproduction. OK?
ReplyDeleteNot OK.
If element A is useless now how can there be any selection for it, other than a negative selection (probably very small if any) making carriers less prevalent due to the cost of carrying a useless function.
I'm not even arguing from a genetic basis (good thing as I have no background) but from a logical basis and your statement seems to be logically incoherent.
If element A is "useless" (your word) then by definition it can not have any beneficial effects.
If Larry were a cosmologist ,heaven forbid, he would be arguing that dark matter and energy (that make up 96% of the universe) were simply "junk".
ReplyDeleteDark matter mirrors dark genomes
I think that pretty much sums up his approach.
Atheistoclast said on Junk & Jonathan: Part 3—The Preface,
ReplyDeleteI completely agree with Wells.
Moran is wrong.
His argument is essentially an argument from personal incredulity and poor analysis.
Thanks for clearing that up.
Now I can ignore you with a clear conscience.
Goodbye.
Steve wrote:
ReplyDeleteIf element A is useless now how can there be any selection for it, other than a negative selection (probably very small if any) making carriers less prevalent due to the cost of carrying a useless function.
You don't understand. Element A may have no use at present but it could do in the future - that is the nature of variation. Therefore, its preservation is beneficial in the evolutionary long-run.
If element A is "useless" (your word) then by definition it can not have any beneficial effects.
At the moment. But in the future it might. Therefore, my argument is that in the future those individuals with in-tact element As will be reproductively better off compared to those with degenerate elementAs.
For example, if some LTR retotransposon is doing nothing at the moment in some obscure part of the genome but relocates to a become a new cis-regulatory element in some gene 100 years from now, then selection will favor those individuals who possess the functional element compared to those who have lost it or have let it become defective.
Larry, unfortunately, can't even begin to understand this. The reason is that he is not a population geneticist - he is a biochemist. That's all he is, that's all he'll ever be.
Jud wrote:
ReplyDeleteWhat unmitigated junk, pun fully intended. I must have something with no benefit (or deleterious) because someone else does, and that leads to an "arms race"? So if my neighbor is in hock up to his eyeballs, I better accumulate massive debt as well or be left behind?
OK...perhaps an analogy would be useful. Say I invest in a backup to my hard drive and you do not. We are both given some deadlined assignment to do on our computers that we both save every night to our respective HD.
Now, one night 2 weeks down the line we both experience some physical failure and we lose the data on our hard drives. However, my backup has been storing all of my data all along.
As a result, I am at an advantage over you since you have to start all over again whereas I don't.
This is one reason why duplicate genes become accumulated in the genome. They may not offer anything beneficial per se other than it always is good to have a backup - those who don't are at a disadvantage compared to those who do.
@Atheistoclast
ReplyDelete"You've been told *over and over* again, Larry, that just because you don't know the exact function of something doesn't make it junk."
Conversely, just because you can imagine a function for something doesn't mean it evolved for an adaptive reason.
A function can be imagined for anything, it's just an exercise in speculation, and very little to do with actual science.
Proud to read that centromeric DNA is considered functional, even though it is not.
ReplyDeleteVarious articles have shown that the kinetochore can form on unique (non-repetitive) DNA. One chromosome in orangutan lacks alpha-satellite DNA, as does one chromosome in horses, whereas most chromosomes in chicken lack repetitive DNA at the centromeric locus all together. In addition, neocentromeres (centromeric relocalizaton on a chromosome) formation in humans happens relatively frequent (in term of evolutionary time), although it is commonly associated with clinical manifestations.
At the same time, tandem repeat arrays have been observed on holocentric chromosomes (lacking a primary constriction or regional/localized centromere), which (currently) have not been shown to associate with kinetochore/centromere function.
For these reasons, I would argue that your estimations of functional DNA in our genome is overestimated by 2%.
I would appreciate dr Moran's comment on:
ReplyDeleteTitle: Transposable element insertions have strongly affected human evolution
Author(s): Britten RJ
Source: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Volume: 107 Issue: 46 Pages: 19945-19948 Published: NOV 16 2010
Dr. Moran, I was looking at your list in your post.
ReplyDeleteWhere do chaperone proteins fit into the picture? Are they produced by coding DNA or non-coding DNA.
Which of your categories does the DNA which produces chaperone proteins fit?
I have a question about this part:
ReplyDeleteProtein-encoding genes: (9.6% junk)
transcribed region:
essential 1.8%
intron junk (not included above) 9.6% d
dIntrons sequences account for about 30% of the genome. Most of these sequences qualify as junk but they are littered with defective transposable elements that are already included in the calculation of junk DNA."
Are you saying that the introns within coding DNA is "junk"?
I have asked:
ReplyDelete"Are you saying that the introns within coding DNA is "junk"?"
Is this too difficult a question to answer?
CORRECTION:
ReplyDeleteWell it looks like Moran is not interested in discussing this further. But it is worth looking at.
Moran covers the topic of introns in this thread:
http://sandwalk.blogspot.com/2011/05/junk-jonathan-part-7chapter-4.html
From there we get the distinct impression that Moran considers introns in protein-encoding genes to be "junk".
And he appears to think that this "junk" constitutes 9.6% of the genome.
Why consider introns to be junk?
Do they perform no useful function?
It seems that they perform the function in the gene of separating the exons. That seems useful. The exons can be distinguished from each other by these separators.
It seems Moran considers them junk because they are spliced out in the process of transcription to RNA.
I wonder if that is why Moran considers them "junk".
It would be great if he could explain his thinking about that.
anonymous says,
ReplyDeleteIt would be great if he could explain his thinking about that.
I do not believe that all introns sequences are junk.
IDiots Do Arithmetic a Second Time - Same Result
Junk in Your Genome: Intron Size and Distribution
Junk in Your Genome: Protein-Encoding Genes
All these links can be found in Genomes & Junk DNA. Anonymous would know that if he had bothered to do any homework before commenting.
But who am I kidding? IDiots don't do homework! That's why they're IDiots.
I am talking about the introns in protein-coding genes.
ReplyDeleteIt appears that Moran considers those particular introns (in protein-coding genes) to be "junk".
It appears that he considers those particular introns (in protein-coding genes) to be 9.6% of the entire genome.
I am hoping he can explain why he thinks that they are "junk". None of his other posts address this question.
The question might be better put as:
ReplyDeleteWhy are "introns" considered to be a percentage of the genome?
Are introns part of the genome?
Evolution theory is left with the odd idea that the exons in the gene are perfectly organized to provide the RNA and then the proteins for the functioning of the creature.
ReplyDeleteBut right beside all these exons are introns that are just "junk".
Please explain using evolution principles such as drift, mutation, selection etc how in the world that could happen.
How can people in this field, not have an answer to the basic question about the existence of "junk" introns in protein-coding genes?
ReplyDeleteThat is about as basic as it gets.
@Anonymous Tuesday, June 07, 2011 6:03:00 PM
ReplyDeleteYour reading assignment.
http://www.genetics.org/content/101/3-4/519.long
http://www.nature.com/nature/journal/v315/n6017/pdf/315283b0.pdf
http://www.imb.uq.edu.au/download/large/Introns_1994.pdf
http://www.sciencedirect.com/science/article/pii/S0960982204002957
http://www.nature.com/nrg/journal/v7/n3/full/nrg1807.html
http://www.sciencemag.org/content/330/6006/920.full
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature09992.html
http://www.biology-direct.com/content/1/1/22
When a difficult question arises about evolution theory, Moran just goes quiet. As does everyone else.
ReplyDeleteAs if by ignoring issues they will go away.
Anonymous, I appreciate that you have taken the time to list some references.
ReplyDeletePlease copy and paste from them the sentences that you think are relevant to the discussion.
I used to read references people gave, only to find that my time had been wasted. I do not do that any more.
You could start by just taking one of them.
Question:
ReplyDeleteWhy would anybody call genetic elements that actually and actively participate in inducing variation in offspring JUNK DNA?
I really don't get that, Mr Moran? Isn't variation a very relevant parameter in evolutionary processes?
A better name for these highly repetitive genetic elements, which affect gene expression through position effect and as enhancers/silencers, would be variation-inducing genetic elements.
Variation-inducing genetic elements...remember that name.
Cheers,
Peter Borger, PhD
Furthermore...the idea of ancient virus integrations in ancestral genomes is non-sensical.
ReplyDeleteViruses have there origin in genomes. That is standard textbook knowledge:
http://www.nature.com/scitable/topicpage/the-origins-of-viruses-14398218
The only remaining & possible explanation is found here:
http://blog.drwile.com/?p=1106
Cheers,
PB