There is an approximate 8% excess of Adenine and Thymine above random in the DNA of humans. This suggests mutational bias and/or non-random mutation. If 3 billion coins were found to be 58% heads vs. 42% tails, then the chance hypothesis of a random unbiased coin flip would be easily rejected. The odds of such an event happening are astronomical according to the binomial distribution.
But such an imbalance is reflected in the human genome where:
(Guanine + Cytosine) / (Total Number of Bases) = CG ratio= 42%
(Adenine + Thymine) / (Total Number of Bases) = AT ratio= 58%
Is this due to natural selection?
Well let’s ask it a different way, can selection maintain this if the mutations weren’t biased or non-random? If the mutation rate is hypothetically about 126 point mutations per individual per generation (about Moran and Gruar’s figures), and they all had an a priori probability of 29 Adenine, 29 Cytosine, 29 Guanine, 29 Thymine — that would mean selection would have to select against 8 Guanine and 8 Cytosine, to leave C+G = 42 and A+T = 58. One can of course scale the numbers, but I chose 126 to make the math easier to see.
That’s a whopping 16 mutations per individual that selection has to select against for each generation. Given the Muller limit of mutations is about 1, this falsifies natural selection as the cause for maintaining the low CG ratio unless selection can act in a synergistic sort of way.
What is peculiar however is the CG ratio is different depending on the species. Woese noticed this even in 1961:
THE ratio of guanine plus cytosine to adenine plus thymine (GC/AT) in the deoxyribonucleic acid (DNA) of a given species of a micro-organism is constant, but the GC/AT ratio of different kinds of microorganisms can vary by a factor of as much as five times
and this from wiki:
https://en.wikipedia.org/wiki/GC-content
GC content is found to be variable with different organisms, the process of which is envisaged to be contributed to by variation in selection, mutational bias, and biased recombination-associated DNA repair.[17] The species problem in prokaryotic taxonomy has led to various suggestions in classifying bacteria, and the ad hoc committee on reconciliation of approaches to bacterial systematics has recommended use of GC ratios in higher level hierarchical classification.[18] For example, the Actinobacteria are characterised as “high GC-content bacteria”.[19] In Streptomyces coelicolor A3(2), GC content is 72%.[20] The GC-content of Yeast (Saccharomyces cerevisiae) is 38%,[21] and that of another common model organism, Thale Cress (Arabidopsis thaliana), is 36%.[22] Because of the nature of the genetic code, it is virtually impossible for an organism to have a genome with a GC-content approaching either 0% or 100%. A species with an extremely low GC-content is Plasmodium falciparum (GC% = ~20%),[23] and it is usually common to refer to such examples as being AT-rich instead of GC-poor.[24]
And a curiosity, the Chargaff parity rules:
First parity rule
The first rule holds that a double-stranded DNA molecule globally has percentage base pair equality: %A = %T and %G = %C. The rigorous validation of the rule constitutes the basis of Watson-Crick pairs in the DNA do.
Second parity rule
The second rule holds that both %A ~ %T and %G ~ %C are valid for each of the two DNA strands.[3] This describes only a global feature of the base composition in a single DNA strand.
So we have the DNA that is duplicated via Okazaki fragments the antisense way and the DNA read straight up. I suppose if the 2nd parity rule were violated, we could see an excess amount of G’s or C’s depending the direction we were reading. I suppose parity rule 2 is somewhat unsurprising, except for this fact, that it is occasionally violated:
https://en.wikipedia.org/wiki/Chargaff%27s_rules
In 2006, it was shown that this rule applies to four of the five types of double stranded genomes; specifically it applies to the eukaryotic chromosomes, the bacterial chromosomes, the double stranded DNA viral genomes, and the archaeal chromosomes.[5] It does not apply to organellar genomes (mitochondria and plastids) smaller than ~20-30 kbp, nor does it apply to single stranded DNA (viral) genomes or any type of RNA genome. The basis for this rule is still under investigation, although genome size may play a role.
Is the violation because there is a mutation bias or natural selection or both?
Chargaff parity rules only emphasizes the lack of parity between CG and AT and yet this other strange feature:
Wacław Szybalski, in the 1960s, showed that in bacteriophage coding sequences purines (A and G) exceed pyrimidines (C and T).[6] This rule has since been confirmed in other organisms and should probably be now termed “Szybalski’s rule”.
A valid experimental observation is to see whether there is a real time change in the present day from generation to generation of these various ratios or parities. If for example, Plasmodium falciparum CG content doesn’t change from generation to generation even if the genome mutates, then it would seem to me mutations are biased/non-random or something.
NOTES:
1. the 42% figure was inexact since it the average wasn’t weighted by the size of the chromosomes, but I felt 42% was in the Ball Park. The unweighted average is here:
http://blog.kokocinski.net/index.php/gc-content-of-human-chromosomes?blog=2
Flint,
RobC wrote:
The listed organisms by RobC mischaracterization:
Actually the OP mentions humans too which do have testes and ovaries. 🙄
Humans: low GC, I listed 42%, there are probably other figures, 1-1.5% DNA methylated at CpG sites
Actinobacteria : some have 75% GC some have 37%
Streptomyces: an Actinobacteria, has high GC
Saccharomyces: yeast, has low GC at 38%, almost no methylation (hence RobC was wrong about yeast)
Arabidopsis: plant with low GC at 36% but very high methylation 14% of DNA
Streptomyces are in soil, so the UV explanation for their high GC content makes no sense.
Humans don’t expose there gametes in general to UV so that doesn’t explain low GC content.
Additionally it makes little sense to use UV to explain high GC content and then use UV to explain low GC content especially where the UV can’t reach the relevant DNA!
And then the methylation explanation falls apart in creatures like Sacharomyces which have almost no methylation.
So RobC’s explanations are ad hoc and non-sensical with lots of special pleadings.
I have no problem with the general idea that there is mutational bias and that each species has a different bias than another. That was what the OP argued!
RobC just couldn’t give a sensible mechanism for the mutational bias.
Mutational bias is not necessarily indicative of design, non-randomness might be another story.
But mutational bias differing in each species suggests to me a gap especially in Actinobacteria. Given theses biases, can we even assert common descent as reasonable for the group?
“Your assertion of UV creating high CG in soil bacteria where UV can’t reach them is right up there with the rest of your statements.”
Sal, Sal, Sal…. the title of the paper you cite on Actinobacter is (and I’ll remove extraneous words, so as to allow your limited reading comprehension to get this) is: “…..abundant freshwater Actinobacteria….”
Freshwater. As in look down at the pretty pretty plants growing down below. Do they need…..light…….? to grow.
So we’ve learned from Sal’s reference that there are soil actinobacteria, freshwater actinobacteria, and cosmopolitan actinobacteria. Acinitobacter with nifty UV damage DNA repair systems. And he asks how can they all be different? Darwin?!?
“You’re the one who put the UV and methylated C on the table as an explanation of low CG. And an explanation of low CG is not an explanation of high CG, and you got caught making an utterly stupid remark.”
Yeah, OK. Tenth time. UV primarily makes T-T lesions, so is thought to favor CG rich genomes. Methylcytosine deamination leads to less CG (as observed in organisms that do it). I’ve been fairly kind to you in this thread, but the stupid in it isn’t mine, Sal. Onlookers will confirm.
Your last post goes coin flip statistics. Who is arguing for a random genome? What law of nature says everything is 50/50 in this case? I’ve provided EXAMPLES showing known mechanisms for your ‘bias’. These aren’t intended as comprehensive descriptions of every organism, but they make their point.
And if there is mutational ‘bias’ in the genome of a species with CpG methylation or that is exposed to sunlight, what then? Design by nature?
“why is there such strong bias in one Actinobacteria (with 37% GC, 822 standard deviations) and another Actinobacteria….. ”
You’ve already shown us. Some are soil-living. Some aren’t. Some have DNA repair mechanisms others lack. You do know you’re talking about an enormous and ancient Phyla? Vertebrates are newer and more conserved. Why don’t we lay eggs?
It seems we’ve discovered Sal’s theory of Random Selection and Unatural Mutation.
The best theory so far for high GC in bacteria is Wu theory:
http://asserttrue.blogspot.com/2014/03/why-do-some-bacteria-have-gc-rich-dna.html#
RobC, to Sal:
Confirmed.
LOL RobC. Are you now saying UV makes bacteria have low GC? What’s your story?
You said earlier:
The freshwater Actinobacteria are low GC (37%-50%) relative to other soil Actinobacteria (up to 75%).
Your understanding is totally backward. Keep digging.
Sal,
Actually (if you read the paper you love), many freshwater actinobacter have a high GC content. The exception is noted to have lovely DNA repair mechanisms and sunscreen like pigments. @45, I asked you “Oh, Sal, since you cited the paper on the low GC actinobacter, which I’m sure indicates you read it, why don’t you quote the line about what was found in their genome regarding UV damage?”
???????????????
Sal,
Please let the lesson sink in. This happens again and again.
You make an assertion. Someone more knowledgeable corrects you. Your ego is bruised, so you lash out at them without thinking things through. They continue to correct you as you make mistake after mistake, looking more foolish with each one. You distort your opponent’s position in an attempt to save face, which just makes you look dishonest and petty.
It’s always a disaster, so why do you keep doing it?
“has advanced the notion that high G+C content is due, specifically, to the presence of the dnaE2 gene, which codes for a low-fidelity DNA repair polymerase. This gene, they say, drives A:T pairs to become G:C pairs during the low-fidelity DNA repair that goes on in certain bacteria ”
So in some bacteria….hey wait, haven’t I said ” “….different organisms have different environments (mutational spectra), different mechanisms acting on their DNA and different DNA repair activities in their germlines. So they evolve different GC contents.” like a dozen times now. Thanks again!
The paper in question:
Gee RobC do you not see the bolded word: “low”. You also went out of your way to point out the freshwater Actinobacteria are exposed to more UV than soil Actinobacteria since you said:
Now let’s see what else you said:
So, the soil bacteria have high GC and they aren’t exposed to UV as much as freshwater bacteria (you’re the one who talked about those plants growing from the light).
So are you sticking to your claim?
If that’s the case, why do the freshwater Actinobacteria have lower GC than the soil Actinobacteria since the frewshwater Actinobacteria have more exposure to UV?
Let’s see if Keiths will still defend you now.
Ok Keiths,
RobC said:
So Keiths, would you expect a freshwater Actinobacteria (exposed to UV) to have a higher or lower GC than a soil Actinobacteria (not exposed to UV). 🙂
C’mon Keiths, simple question.
freshwater Actinobacteria : 37-50% GC, UV exposed
soil Actinobacteria: 70-75% GC
Hint : 37% < 75%
Hint: 37% with UV < 75% no UV
Hint: RobC is wrong to make this assertion:
Ok, confession, the real reason I like Wu theory:
Sal,
“If that’s the case, why do the freshwater Actinobacteria have lower GC than the soil Actinobacteria ”
As I’ve said, I don’t believe that is universally true, and the paper you cite makes a big deal about the DNA repair mechanisms and pigments of the freshwater Actinobacter, which you previously described as only soil living, and therefore immune to UV.
Bored now……
What is your point??? No really, besides demonstrating that given years of arguing about biology you’ve learned nothing, and that you’re willing to embarrass and contradict yourself, what is it you have here?
Mutational bias=design=God?
If your next response doesn’t take the form my point is x for y reason, I’m out. It is easy to be a nihilist jerk who just pokes holes and mocks and makes shit up if all else fails. Putting a position forward and defending it is hard. You’ve learned well from your mentor Barry Arrington to stick to the former when you have a weak position or persona.
Sal,
I’ve noticed that you’ve been trying pretty hard lately — for the most part — to behave better than OldSal. There’s been less dishonesty and fewer irrational outbursts. Your ideas are still batshit, and you’re still largely impervious to evidence and reason, but your conduct has at least been better.
Don’t let a little tweak to your ego cause you to undo all of that hard work.
Keiths,
Simple question.
RobC said:
Do you agree or disagree with RobC’s statement?
Sal,
The time for face-saving is before you faceplant, not after.
Meanwhile, you’re just making it worse with quotemining stunts like this:
Here’s what Rob actually wrote, with the parts you omitted in bold:
You really can’t help yourself, can you? The self-control simply isn’t there.
That argument does not fly. Sequence under selection is not evenly distributed through the genome, and nor is GC/AC content, but those mutations (approximately) are. Selection only has to act on sequences under selection. Which, ENCODE aside, appears to be less than 10% of the genome. Coding genes are GC rich, and CpG islands distort the average too.
Yes, yes, I know ENCODE is the absolute incontrovertible God-given PROOF that junk DNA does not exist, but that’s the simple answer to your conundrum, at least as far as selection is concerned (only one component of the bias, of course).
Another factor so far ignored is the role of transposons, which constitute 50% of our genome. If they experience a selective bias (for transposition, not organismal fitness) related to their GC content, this would be amplified every time they transposed. Even stochastic variation would be amplified thus – while stochastic variation may be unlikely to depart from evens in a multi-megabase genome, if that genome is composed of copy-paste repeats of a shorter stretch (a few hundred BP), then the result might appear puzzlingly biased. It’s like tossing a fair coin 10 times, getting a perfectly possible 6H 4T and then copying that sequence a thousand times. Someone unaware of the mechanism would conclude that an apparent run of 10,000 tosses was inexplicably biased to generate 60% heads, well into the tail of the distribution if it really were 10,000 independent tosses.
Is this bias present in junk DNA too?
dazz,
Parts of it. The distribution is very patchy, are there are probably several mechanisms operating. But there does seem to be a mechanism that enriches genes in GC if they are in a GC rich neighbourhood. Even pseudogenes (junk) appear to become more GC rich if they are translocated into a GC rich region. That’s not to say selection isn’t involved in the maintenance of such a region, but it can’t be operating at individual base level. Alternatively, it could simply be biochemistry.
Another factor: gene conversion. During recombination (crossover), a patch of the homologous chromosome is pasted across the break, and during resolution a single strand from one partner pairs up with the complementary strand from the other. When the two chromosomes are not precisely identical, you end up with some mismatched bases, which have to be repaired. This process experiences a bias towards CG.
Precisely. I reckon that this erroneous assumption of independence may be the clearest way to get ID-mathematicians to see the error of their ways. Even Sal must recognize that his “22-sigma” calculations assume that each nucleotide (or coin flip, or amino acid) is independent of all the others; even Sal must recognize that this isn’t true.
OTOH, I doubt that colewd will get my joke about mouse titin being 10^1122 more unlikely than human titin…
According to DiEb’s analysis, you’re the biggest local here (2015)!
I do wonder if it’s possible to distinguish your seagull commenting from substantive responses, though.
It’s the Cordova version of the Gish Gallop — the Sal Scramble.
When you recognize that his goal is not to understand science better but to collect sciency sounding sentences for the purpose of impressing his co-religionists and convincing them to allow him to abuse their children, it makes more sense.
And yes, I do think he’s dedicating himself to that goal in good faith.
It’s the good faith part that’s scary.
That, combined with the theological card counting.
Finally, we get to Sal’s point, which he originally denied having.
Keiths,
It looked to me you were practically slobbering over this statement by RobC earlier:
You said right here
Keiths, help me out here bro, do you agree with RobC’s statement or not?
I can’t tell whether you agree or not. Also do you want me to agree with it or not?
You could say, “Sal, I disagree with RobC’s statement especially in light of your freshwater Actinobacteria counterexample.”
Or you could say, “Sal, I totally agree with RobC’s statement despite your freshwater Actinobacteria counter example.”
Or you could say, “Sal I agree with RobC’s statement because…”
Or you could say, “Sal, I disagree with RobC’s statement because….”
Can you clarify what you believe about this statement by RobC:
The design reason is so obvious, after all.
Just don’t expect Sal to tell us why design called for A and T excesses, or for bird wings fused from many bones, or, well, anything at all.
Baby Jesus just wanted it that way, admit it.
Glen Davidson
Allan,
That might be true for construction (and it would have to be relatively fast), but not maintenance over the long term, which is what Muller’s limit pertains to.
If the mutation repair mechanism is not biased also, the GC bias will erode slowly.
And in any case we have the Actinobacteria with GC ratios going from 37% to 75%. It would seem difficult to argue one mechanism in play for one set of that group that totally doesn’t work for another set, unless Wu theory (the naturalistic one by Hao Wu, related to the presence or absence of a specific gene) is correct. Actinobacteria would be a good test of naturalistic Wu theory.
Whether that Wu theory is right or wrong, I think it is at least plausible. It would be good to see if the dnaE2 gene has any role in the very diverse range of GC in actinobacteria.
Otherwise, one could go with the other Wu theory (the one pronounced Woo). 🙂
Do you know the [Redacted] Meander?
http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?s=56bdf713615b8061;act=ST;f=14;t=8960;st=0
All of this esoteric stuff is just to impress us with how learned you are?
stcordova,
Don’t understand. Transposition, gene conversion, selection, and so on – these are ongoing processes. And Muller’s ‘limit’ is irrelevant in non-selected parts of the genome (which, unless ENCODE put some flesh on their ‘functional’ bones, is the vast bulk of it).
Who says the repair mechanism isn’t biased? In fact, I gave a link that shows that it is biased – the mechanism of mismatch repair tends to increase GC content. The paper referred to repair in meiotic crossover, but in fact the same pathway is invoked in homologous repair in non-meiotic cells too.
But it’s not an either/or – selection OR mutational bias.
stcordova,
What functional reason can you suggest for a Creator coming up with such variation?
“Bias” appears to almost as powerful an incantation as “code”.
Harry Potter science.
I’m waiting for: “if there is bias, how come genomes aren’t 100% GC?”.
The intelligent design creationists are evolving!
Only thing missing is a link to you quoting yourself as confirmation.
Woo theory. I hear that’s real popular here.
Barry must have put his keys in his purse.
To thwart evolutionary explanations and force humans to consider Wu theory (pronounced Woo).
🙂
Nah, this is just glorified coin flip analogies in DNA.
You are aware that coins an dice can be biased and the outcome of tosses still stochastic? Asking why some bit of biology is biased is a legitimate question, and might be interesting coming from someone actually researching the problem.
Coming from you, not so much. Your agenda poisons everything you touch. Everyone assumes there’s a gotcha lurking behind everything you say, and I’d say this suspicion is justified.
It’s interesting that not only do the theists have a religious agenda behind all they write, but they can’t help but regard a fact-and-explanation oriented agenda as being unavoidably distorted by the religion of atheism. Religious spectacles, once branded on, can’t be removed.
stcordova,
If he’s trying to thwart evolutionary expectations, he’s doing a crap job, given at least 3 different and non-exclusive evolutionary mechanisms for producing a bias.
Yes, atheism is a religion and it’s adherent’s have an agenda.
Finally! Honest petrushka!
Atheist spectacles come cheap.
Everyone knows that what theists and IDists write here at TSZ is colored by the glasses worn by the atheists and anti-IDists here at TSZ and that this affects whet they read. Let’s drop the pretense that you all are the “objective” ones.
How about whales?
Quite so. Theists wonder how they can insert the supernatural entity of their choice into everything on the grounds that they can’t help believing it’s there. Non-theists wonder how they can produce the most predictive explanations based on the observed facts, assuming no supernatural dicking with reality.
The theists had about 4000 years to apply their approach, and got essentially nowhere. The non-theists have had less than 10% of that time, and have made advances that have revolutionized everything. These may look identical to you, but others may disagree. Subjectively, of course.
You don’t actually believe this though. You have to keep hanging on the your unchanging dogma that intelligent design is creationism based on some changes made to a book way back when. It’s like you believe in types and a single homologous feature that defines what it means to be an intelligent design advocate.
The clear evidence, from the intelligent design creationists’ own writing, is that “intelligent design” and “creationism” are synonyms. Nothing has changed since the Dover trial to change that.
In fact, very little has changed with respect to IDC at all in the past ten years. There’s still no scientific hypothesis of ID, still no testable entailments that could either support or disprove such an hypothesis, no evidence whatsoever. All the IDCists have is arguments from incredulity and the frantic desire to disprove evolution so that their religious beliefs can win by default.
Intelligent design is a variant of creationism.
The defining feature of all the various flavors of ID is belief in some sort of foreknowledge. Some way of anticipating the results of genomic changes, and presumably of effecting desired changes.
Exactly how this happens, or what the designing entity might be, is irrelevant.
Although, by some strange coincidence, most ID advocates spend a lot of time talking about religion, disparaging atheism and materialism, and so forth.