Theme
Mutation
-definition
-mutation types
-mutation rates
-phylogeny
-controversies
Let's review what we know. The first thing we have to do is define "mutation" [What Is a Mutation?]. A mutation is any alteration of the nucleotide sequence of a genome. It includes substitutions, insertions, and deletions.
The mutation rate can be described and defined in many ways. For most purposes, we can assume that it's equivalent to the error rate of DNA replication since that accounts for the vast majority of substitutions. Substitutions are far more numerous than most insertions and deletions. (But see, Arlin Stoltzfus on The range of rates for different genetic types of mutations).
One kind of rate is the error rate of DNA replication. This is close to 1.0 × 10-8 for replication complexes that are capable of proofreading. Many errors are repaired by repair enzymes and this process is about 99% efficient. Thus, the overall error rate is close to 1.0 × 10-10 per bp.
Given that the human genome is 3.2 × 109 bp, this means that there are on average 0.32 new substitutions every time the complete genome is replicated. In humans there are about 30 cell generations between zygote and egg cells and about 400 cell divisions between zygote and mature sperm. Thus, in males, the sperm cells have about 128 new mutations and the haploid egg genome has about 10 new mutations for a total of 138 new mutations in every new zygote. Let's round this down to 130 mutations per generation.1 I call this the "biochemical method" of calculating mutation rate [Estimating the Human Mutation Rate: Biochemical Method].
This is a pretty reliable number. The error rates of DNA replication and repair are well-studied and they are unlikely to be off by more than 20%. The number of cell divisions per generation is less reliable but still pretty accurate. The number of divisions during spermatogenesis varies with the age of the father so that that older men pass on more mutations but the number used here (400) is a good average. The overall mutation rate of 130 mutations per generation is likely to be close to the actual mutation rate.
The second method is something I call the "phylogenetic method" [Estimating the Human Mutation Rate: Phylogenetic Method]. It's based on the idea that the vast majority of mutations in primate genomes are in junk DNA. That means they are neutral. If we compare the genomes of different primate species, we can calculate a mutation rate based on population genetics, which postulates that the rate of fixation of neutral alleles is the same as the mutation rate.
This gives mutation rates of 112-160 mutations per generation. That value depends on knowing the time of divergence of different lineages (e.g. humans and chimpanzees) and the generation times. Both of these values are subject to uncertainty but they can't be off by very much. Certainly not by a factor of two or more.
The third method is the "direct method" [Estimating the Human Mutation Rate: Direct Method]. This is where you sequence the genomes of parents and their offspring or you sequence the genomes of two individuals who descend from a common ancestor. All you need to do is count the number of new mutations and you get the mutation rate directly.
These experiments yield a range of values from a low of 56 mutations per generation to a high of 103 mutations per generation. Most of the values cluster around 75 mutations per generation and that's what gives rise to the controversy. The direct method gives mutation rates the are about half the rate of other methods.
The direct method is not very reliable since the quality of the genome sequences is low and only a fraction of the genomes is actually sequenced. Typically about 60-80% of the genome sequence is reliable. The number of potential sequencing errors overwhelms the number of possible mutations so a lot of "adjusting" is necessary in order to weed out false positives and false negatives. Nevertheless, it's satisfying that the results are in the right ballpark.
Geneticists ... are having trouble deciding between one measure of how fast human DNA mutates and another that is half that rate.This is a bit of an exaggeration. The main problem comes from interpreting the direct measures of the mutation rate and those number aren't really "so much lower" than previous estimates.
The rate is key to calibrating the ‘molecular clock’ that puts DNA-based dates on events in evolutionary history. So at an intimate meeting in Leipzig, Germany, on 25–27 February, a dozen speakers puzzled over why calculations of the rate at which sequence changes pop up in human DNA have been so much lower in recent years than previously. They also pondered why the rate seems to fluctuate over time. The meeting drew not only evolutionary geneticists, but also researchers with an interest in cancer and reproductive biology — fields in which mutations have a central role.
But even a twofold difference is cause for worry if the mutation rates are used to determine the history of human evolution.
Later estimates of the mutation rate counted the differences between stretches of DNA and protein amino-acid sequences in humans and those in chimpanzees or other apes, and then divided the number of differences by the time that has elapsed since the species’ most recent common ancestor appeared in the fossil record. These estimates were clouded by the patchiness of the fossil record, but researchers eventually settled on a consensus: each DNA letter, on average, mutates once every billion years. That is a “suspiciously round number”, molecular anthropologist Linda Vigilant of the Max Planck Institute for Evolutionary Anthropology in Leipzig told Nature in 2012 (see Nature 489, 343–344; 2012).The human diploid genome consists of 6.4 × 109 base pairs (6.4 billion). That works out to 6.4 mutations per year. The average generation time for humans is 30 years so that means 30 × 6.4 = 192 mutations per generation. That's very much on the high end of estimates that I've seen.
In the past six years, more-direct measurements using ‘next-generation’ DNA sequencing have come up with quite different estimates. A number of studies have compared entire genomes of parents and their children — and calculated a mutation rate that consistently comes to about half that of the last-common-ancestor method.This is correct. The direct measurements generally turn out to be lower than the estimates made by other methods.
A slower molecular clock worked well to harmonize genetic and archaeological estimates for dates of key events in human evolution, such as migrations out of Africa and around the rest of the world1. But calculations using the slow clock gave nonsensical results when extended further back in time — positing, for example, that the most recent common ancestor of apes and monkeys could have encountered dinosaurs. Reluctant to abandon the older numbers completely, many researchers have started hedging their bets in papers, presenting multiple dates for evolutionary events depending on whether mutation is assumed to be fast, slow or somewhere in between.The problems aren't as severe as this implies. If the average mutation rate is about 130 mutations per generation then this is consistent with a human-chimpanzee split about 5-6 million years ago. If the actual rate is only 75 new mutations per generation then this pushes the last common ancestor back to about 10 million years ago assuming that the generation times are accurate.
This older value is probably not right so the actual mutation rate is likely to be more than 75 mutations per generation.
This seems like a problem but there are all kinds of potential errors in these calculations. For one thing, we don't know how accurate the Denisovan sequence is and what the real number of differences are. There are also issues with population sizes and actual times of divergence, not to mention generation times.
There's no point in getting your knickers in a knot at this time.
Last year, population geneticist David Reich of Harvard Medical School in Boston, Massachusetts, and his colleagues compared the genome of a 45,000-year-old human from Siberia with genomes of modern humans and came up with the lower mutation rate2. Yet just before the Leipzig meeting, which Reich co-organized with Kay Prüfer of the Max Planck Institute for Evolutionary Anthropology, his team published a preprint article that calculated an intermediate mutation rate by looking at differences between paired stretches of chromosomes in modern individuals (which, like two separate individuals’ DNA, must ultimately trace back to a common ancestor). Reich is at a loss to explain the discrepancy. "The fact that the clock is so uncertain is very problematic for us," he says. "It means that the dates we get out of genetics are really quite embarrassingly bad and uncertain."Of course the direct measurements are going to be uncertain because you are sequencing individuals. These are not "finished" sequences that have been edited and corrected.
My view, is that the direct ("genetic"?) mutation rates are probably systematically low and the real rates will likely be more than 100 mutations per generation.
1. I'm rounding down to be consistent with other posts on this subject.
Meyer, M., et al. (2012) A high-coverage genome sequence from an archaic Denisovan individual. Science 338: 222-226.
197 comments :
Does this imply that males contribute about 12 times as many mutations to the next generation as females, or is this ratio possibly diminished by the fact that only the healthiest sperm are likely to be successful?
Or something else?
@Petrushka. Yes, many more of the new mutations we inherit arose in our fathers than in our mothers. Very few of these mutations will be weeded out by selection for sperm success, both because very few are in functional sequences and because the proteins responsible for sperm function are mostly made from the parent's complete genome rather than the single set of genes in the sperm.
Continuing a possibly dead end line of thought, could sex contribute to evolvability by increasing the number of mutations in population while simultaneously providing a "back-up" of critical genes. It sounds to me a bit like a corporation having a radical research and development team at work on high risk projects while maintaining cash flow from established products.
I can be carried away bey analogies and metaphors.
Petrushka: you seem to be talking not about sex but about ploidy.
I'm talking over my head, and hoping that someone will help straighten me out.
I think it's interesting that males contribute ten or more times more mutations to a population than do females, and I wonder if this is adaptive.
The average generation time for humans is 30 years so that means 30 × 6.4 = 192 mutations per generation.
The "sage-iest" of all sage authorities, Wikipedia, in its article for the term "Generation," says generation time approaches or even reaches 30 years in modern developed nations. Would you have a tremendous problem with a shorter generation time through most of human evolutionary history, which using your formula above, seems to work out to a mutation number much closer to that obtained through the "biochemical method"?
No, it isn't adaptive. It's simply a consequence of the number of cell replications in the germ line, and that's simply a consequence of the much greater production of sperm than of eggs. It could conceivably be exaptive. But in what way?
One might add to all this (very good) discussion that if the human/chimp divergence is pushed back closer to 10 Myr than 5Myr, this has interesting implications for interpretation of fossil such as Orrorin (about 6 Myr) and Sahelanthropus (perhaps 7Myr). These show signs of bipedality, though there is some controversy about that.
If the chimp-human split is earlier, then there is no immediate need to consider the chimp-human common ancestor to be bipedal.
Any replicating system must be copying almost perfect from the start otherwise it would meltdown immediately.
What I am still interested in is what I raised in another thread after someone replied as follows: "We have moved on beyond Darwin, while idiots like yourself are stuck with Darwin's name, and even then, you oppose it without understanding any of what that guy proposed. You're opposition is mere stupidity trying to pass for science."
What I am really interested in is the whether modern evolutionists have come up with anything in addition to selection that can explain an increase of genomic information, which must have taken place from microbe to man evolution.
Personally, I think all information has been around since T0. Selection is mere there to conserve.
Not the healthiest, the most energetic. There would be selection only on the swimming capacities of sperm cells. Te rest is dragged along. Imagine that during a bottle neck (Noah ark, or so) one sperm with a peculiar genetic make up won the race...instant evolution.
There has also been this other upright walking ape...15 million years ago....maybe that helps.
http://www.sciencedaily.com/releases/2007/10/071009212545.htm
I noticed that the actual evidence for mutation rate is very scanty and there is no mention of the genetic load. 100 mutations per generation is an estimate as good as anyone's at 200 or 300. I fail to see why it can't be 50 or as high as 500
I was at that meeting and the concensus is that the best point mutation for humans is 0.5 x 10^-9 mutations per base-pair per year. Self citation: http://dx.doi.org/10.6084/m9.figshare.1319616
Great! You must have the hardcore evidence rather than BS estimates.
Let's see it Larry can't wait. It is his favorite subject
Cartwright, have you ever watched a Seinfeld episode in the Chinese restaurant???
Extrapolating backwards is guessing based on , at best, present rates.
there is no reason to see these mutations as the samne now as in the pass.
No reason to see they make a difference even if true as far as the simple scenarios shown here.
If a chimp/man connection is guessed at then why not predict the future changes.?
Hard to believe that in the era of NGS geneticist still organize conventions to estimate the Mutation Rate in humans.
Must be the free pretzels and beer.
The 1000GP project was pretty clear.
Thanks for bringing this paper up, which I somehow missed. It looks to be exactly the kind of fossil evidence we need for a split of human and pongid at 18 million years ago, as was found by DNA evidence described in my 2012 paper.
Huang, S. (2012) Primate phylogeny: molecular evidence for a pongid clade excluding humans and a prosimian clade containing tarsiers. Sci China Life Sci, 55: 709-725.
Early Apes Walked Upright 15 Million Years Earlier Than Previously Thought, Evolutionary Biologist Argues
Date:
October 10, 2007
Source:
Public Library of Science
Summary:
An extraordinary advance in human origins research reveals evidence of the emergence of the upright human body plan over 15 million years earlier than most experts have believed. More dramatically, the study confirms preliminary evidence that many early hominoid apes were most likely upright bipedal walkers sharing the basic body form of modern humans.
Petrushka - sex does contribute to evolvability, but in a more roundabout way than gender differentials, which are simply a consequence of differential cell divisions (a gap that widens with the age of the parent). Many species do not have such a differential, and adaptive theories on mutation rate generally tend not to fly.
But the recombinational element of sex allows for 'distributed processing' of the notional search for solutions to Life's problems. The better solutions are integrated in mosaic genomes. Without recombination, genes are chained together in indivisible lumps which selectively interfere with each other, slowing things down and working against character optimisation. Which is not, I should emphasis, a 'reason' for sex, but a consequence of it.
What, the entire genomic sequence of modern life was present at the start? How did selection conserve the giraffe part, the adder part, the dandelion part etc, while those phenotypes were unexpressed?
The average generation time in my ancestral lineage from 800AD is 28 years. Lots of studies suggest that this hasn't changed very much in recorded history.
The average generation times for gorillas and chimps is comparable suggesting that this has been the correct value for several million years.
That's about 96 mutations per generation. What was the consensus view on the source of error in the biochemical calculation?
What I'm really puzzled about is how scientists estimate the different--in many cases much different--mutation rates in different organisms in Cambrian Explosion and most of all what caused them
Thank you for this post, Dr. Moran. I'm an ID proponent but I enjoy reading your blog. When you leave out the name calling, you're an excellent science and can have a knack for communicating complex topics to laymen.
I had been linking to your previous blog posts on the human mutation rates for when people asked me about it--it's nice to have them all together in one place.
Do they? Do you mean mutation rate or substitution rate?
The information was present, i.e. the genes, not the context in which these genes are expressed. The context is determined by the gene order and regulated by what has been coined junk DNA, which in fact makes a sort of morphogenetic road map. The entire sequence, the context in which the genes are expressed, as we observe it today, is determined by a mechanical proces (often called evolution), which is the plastic part of the genome. It has all been frontloaded. All new biology data proof it.
Lets see, if you can name a gene that makes the long neck of the giraffe?
You cannot because no novel genes are involved. It is not a gene, but a network of genes in a sea of regulatory TEs that as a holistic szstem determined longneckivity. All that is required is a novel context of preexisting information, which puts the genes in a novel 3D genetic regulatory environment.
And that is accomplished in a few generations. Reshuffling the genome through action of TEs is sufficient.
Now let me repeat myself: dear professors and other in Darwin educated people:
What else is there to drive an increase of genetic information apart from darwinian selection....
These is nothing. Because genomes were frontloaded.
Prof Moran, tell me, what else is there in modern evolutionism, apart from selection, that enables the formation of novel genetic information?
Explain the bottle drifting in the ocean...
Or did we not move beyond Darwinism ?
You are a prof so please educate us.
Gnomon,
The issue is that the genes were already present from the start. The context to walk upright can be expected to emerge over and over.
It explains why we observed convergence&homoplasy all over.
Later estimates of the mutation rate counted the differences between stretches of DNA and protein amino-acid sequences in humans and those in chimpanzees or other apes, and then divided the number of differences by the time that has elapsed since the species’ most recent common ancestor appeared in the fossil record.
This carries two possible errors, one of which is almost silly (but relevant) and one that is not silly at all (but also relevant).
1) If you count the number of differences between two sequences and divide this by the time since the MRCA, you get ~2µ, because both lineages have been changing. This is rather obvious, but it's also something people messed up, because some papers using phylogenetic estimates give divergence rates rather than mutation rates and that's something that has slipped by researchers and sometimes reviewers as well.
2) The FAD for the MRCA may be off, because the fossil record does not have perfect temporal sampling. There are good practices for using fossils to calibrate trees (and some work is done on improving them), but the key is not to rely on a single fossil for this.
So it is your contention that the entirety of all protein coding genes required for all of life was front-loaded in some primordial species, thousands of them having no function in whatever weird organism you think must precede us all, and they were all magically maintained until they were suddenly expressed 2 billion years later or however long it took?
"What else is there to drive an increase of genetic information apart from darwinian selection...."
Mutation and genetic drift. It really is trivially easy to see how mutations can rewrite genetic sequences into new ones with accumulating mutations. That's it, that's how genetic information is increased. You are inventing a problem that doesn't exist.
That failure is yours then.
"tell me, what else is there in modern evolutionism, apart from selection, that enables the formation of novel genetic information?"
Mutation and genetic drift. It really is trivially easy to see how mutations can rewrite genetic sequences into new ones with accumulating mutations. That's it, that's how genetic information is increased. You are inventing a problem that doesn't exist.
"So it is your contention that the entirety of all protein coding genes required for all of life was front-loaded . . . and they were all magically maintained until they were suddenly expressed 2 billion years later or however long it took?"
Yes, Mikkel, that does seem to be PT's thesis, though even he realizes that those front-loaded genes would mutate to nonsense in 2 or 3 billion years. His solution: earth and all living things are only a few thousand years old. Viola! No problem.
(Well, maybe a problem or two, or twelve, or hundreds, but PT doesn't seem disturbed by them.)
Oh, well it's not just evolutionary biology Peer has a problem with then. It's nothing less than all of science.
And this recombination does not always require a contribution from another individual. Many ciliates when stressed will undergo autogamy which is essentially sex without a partner. Ciliate masterbation, if you will. The cell undergoes meiosis and then recombination with itself.
Mmmm, but there are 2 genomes in there somewhere! Still, it needs a population and outcrossing to allow the finer-scale genomic subdivision and integration to which I refer. Autogamy increases homozygosity across the entire chromosome (as does recombinational gene conversion in asexual diploids).
The information was present, i.e. the genes, not the context in which these genes are expressed. The context is determined by the gene order and regulated by what has been coined junk DNA, which in fact makes a sort of morphogenetic road map.
That doesn't really answer the issue. Shuffling unexpressed genes does not preserve them, and TEs themselves are not so benign as to solely insert themselves between ORFs - they are mutagenic.
The significant character of a giraffe which distinguishes it from a dandelion is not contained solely in the neck. No-one is arguing 1 feature=1gene. There is a mixture of regulatory, gene order and coding difference between any 2 species.
TEs seem to appear, flourish briefly in a clade and then decompose. Some get incorporated into coding or regulatory sequence, and some are involved in gene order changes, sure. That's called mutation, of which there are numerous sources besides.
What is the distinguishing characteristic of 'new' information - how would you distinguish it from 'old', if someone were to propose a mechanism to answer your challenge?
As usual this isn’t a scientific issue, but a religious one.
The real problem here is that Peer considers a few vague sentences in the bible as constituting the alpha to omega of fundamental scientific knowledge. Somehow, in a completely undefined way, an omnipotent entity was able to create all genetic information in a single flash of instantaneous and comprehensive chemistry. Presumably, this entity would also be powerful enough to construct an evolutionary process following the natural (god-made of course) laws of physics and chemistry too. But, despite the overwhelming appearance of slow molecular evolution, the omnipotent creator didn’t do it this way, because this is not what Peers was taught in Sunday school, and he can’t reinterpret any vague sentences in the bible to support that view.
For the rest of us, many of whom also attended Sunday school, we now notice that these stories were made for children, and their intellectual kin.
I am bewildered be the frequent references to a hypotheticaal problem of the generation of new information. AFAIK, we have several mechanisms, like horizontal gene transfer, gene and even whole genome duplication. Plus the ubiquitous mutations.to any part of the genome
Hi Joe
I keep hearing different values for Human Chimp divergence.
However, this story is confusing because interbreeding between Chimps and Humans continued for millions of years (no differently than currently with Dogs and Wolves) creating hybrid-species.
In other words, the Hominidae story is no different in kind than the Canidae story, the former merely has a head start on the time scale according to my limited reading on the subject.
The important bit, in evolutionary terms: would be that the common ancestor in both scenarios is long extinct! This is a very important distinction when trying to talk to Creationists!
However, this all throws into confusing question what exactly would be meant by the term "species" and by the term " last common ancestor".
I remain confused as usual.
http://www.livescience.com/783-human-chimp-ancestors-interbred.html
So Peter Borger - do you still believe that your "analysis" of one exon of one gene trumps whole genome comparisons? You should stick with your asthma research, where you might at least have some recognized competence. Your creationist views make your musings on other areas seem like the rantings of a spoiled child.
Ah - Noah's fake ark. Tell us all Peter Borger, asthma researcher - how did they store all the food needed for the elephant kind on this giant wooden boat made by non-sea faring folk of advanced age?
So Peter Borger - if the genes for bipedality were there all along, please explain (and provide evidence for) the mechanism by which these genes' expression was repressed in so many species for so long, and what these genes are.
Peter Borgher - please DEFINE "genetic information" in a relevant, meaningful, biologically-relevant way. Front loading is a fool's hypothesis, for it requires far more "information" on how to repress the exprtession of hundreds of genes while keeping them extant for millenia. The problem with creationists with biology backgrounds is that they fail to realize that their religious musings do not translate so well into areas of research distant from their own. Tell us all Peter - how many front-loading and creationist concepts do you employ in your asthma research?
Peter Borger - still waiting for you explanation as to how all the necessary genes were front loaded, by whom, and how the un-used genes remained viable for so many millenia. What real mechanism can explain this? Surely, with your expertise gained by looking at single exons to disprove evolution you will know the TRUE genetics that explains your thesis, yes?
Manning, do you have any specific question? I do all question on molecular biology, genetics of complex diseases, the role of TEs, asthma included, etc. And I could speculate a bit on Noah-s ark if you wish...
Food storage was on the upper deck. Plenty of space left, if you realize that 90 percent of all kinds (even today) was not bigger than a rabbit. Dinosaurs went in as babies .....zou didn-t know that?
And please refer to me as Peer Terborg (have some very bad experience with some nasty atheistists at my previous uni...life is tough for antiDarwinian scientists nowadays).
Prof Moran, can you make sure my name is erased from Mannings mails. Thanks.
Please refer to me as Peer. I need this pseudonym for safetz reasons. Otherwise I have to stop posting here.
The genes for upright walking are rather genes in a morphengenetic regulatory network, but we do not know all individual members. It is stupid to think in terms of single genes to explain complex traits. The reductionary approach is deadwrong. Complex traits such as upright walking cannot be reduced to single genes. Upright walking requires integrated coregulated genetic circuitry.
Everybody knows that I am Dr. PB, so there is no need to spell it out. Don/t be a child.
I see some excellent responses. Frontloading is indeed the only way to explain biological evolution...
To stabilize frontloaded information for eons is impossible and therefore the eons have never existed. It is a Lyell/Darwin invention who required it for their gradualism. Evolution is hower not a gradual process as we all know from the fossil record. Of course, Creator could have chosen to code in another frame to stabilize frontloaded info.
Furthermore, I propose not one single frontloaded created kind, but many. Probably as many as there are genera.
And Manning, can you now stop naming me PB. We all know I am PB, but for safetz I would like not to have my pseudoname exposed. Thanks. And ask the Nature and Science editors for a definition for info, they write about it all the time. I am sure you know what they mean...I mean the same.
Tell us all Peter - how many front-loading and creationist concepts do you employ in your asthma research?
All of medical research is research on the preexsiting and what can go wrong if mutations occur in the preexisting. Whether or not the preexisting was frontloaded or not is completely not relevant. What I know from my asthma studies is that evolution is never required to understand the data.
Mikkel, you already started with code. Code is only stabilized when it is essential to the reproduction of an organisms. That is what you call selection. Selection is merely conservation of preexisting code. Now I ask for new code without selection and you say mutation. But you need selection immediately to conserve those mutations, and that can only be done if they positively affects repruduction. So mutation is not the mechanism. Mutation is the variation of Darwin which can be selected. A mutations may also drift for a while, but for an complexity increase selection is required. Drift no new genes make.
So, there is nothing but selection. Modern evolutionism never moved beyond Darwin.
Whole genome duplication hypothesis prior to the evolution of vertebrates, the socalled 2R hypothesis, was falsified over and over by observations on the genomes. Plenty of literature abvailable.
And HGT is merely explaining away obserations that otherwise would falsify known lines of descent.
The real problem is that evolutionism cannot be falsified with the introduction of such concepts. Homoplasie, convergence and HGT (the use of known genes in an unexpected context) all point to ID, but this conclusion cannot be allowed.
Try frontloaded evolution. It explains it all....and better than the current ideas.
Hey Peer,
Don't you post as Peter Borger on creation.com and scienceforums.net to name a few ?
Why so shy here and not there ?
You do know that the Internet is connected by a bunch of tubes, don't you ?
What are the "safetz" issues that have you so worried ?
And how much food do you think was stored was on the upper deck of Noah's ark and how do you come up with this figure (an approximate answer would be fine) ?
Would you say that your worries about "safetz" are proportional to the absurdity of the ideas you publish ?
Do you think if we continue calling Peter Borger Peter Borger and refrain from worrying about his safetz issues he will stop coming?
It depends a lot on whether it’s through the male or female line, or a mixture. The longest male lineage has an average of 38 years/generation for me, and the longest female lineage has 25 years/generation. However, those are both quite short (5 and 4 generations respectively). The longest lineage I can find gives 26 years/generation (26 generations from 1270 to 1943).
@Peer Terborg
Your whining for getting your name erased is even more pathetic than your 'insightful' comments.
It is even more ridiculous keeping in mind that you tend to spam the threads with links to your scribblings in "Journal of Creation ".
Is that some kind of hind-loading vanity ?
Or do you seriously hope to generate some citations for your frontloading-BS ?
@"PeerTerborg"
Now that you are 'exposed': See it positive!
Maybe you can join the casting for the sequel of "Expelled":
"Expelled II: Absolutely no Intelligence allowed"
Maybe a new direction for your career ?
P.S: Nice pseudonym!
https://www.youtube.com/watch?v=H4FdP42cJU0
It is all well and good that you want to try to claim that 90% of all "kinds" were the size of a rabbit - but I am pretty sure that no "kinds" of elephants, bison, cattle, etc. were the size of a rabbit. I have seen calculations demonstrating that nearly 2/3 of the ark's volume (and this is NOT including structural supports, decking, etc.) would have been needed JUST for food JUST for the 'elephant kind'. Your unquestioning acceptance of religious myths is nearly as pathetic as your pretense at understanding population genetics and phylogenetics.
So 'Peer' - why did you feel the need to misrepresent me? I did not write or imply a thing about a single gene. What is stupid is how frequently creationists feel the need to lie to prop up their nonsense.
Please address what I actually wrote:
"if the genes for bipedality were there all along, please explain (and provide evidence for) the mechanism by which these genes' expression was repressed in so many species for so long, and what these genes are."
Thanks Petey - you just proved that your own pet fairy tale (front loading) is an absurdity.
"if the genes for bipedality were there all along, please explain (and provide evidence for) the mechanism by which these genes' expression was repressed in so many species for so long, and what these genes are."
Thanks Petey - you just proved that your own pet fairy tale (front loading) is an absurdity.
"if the genes for bipedality were there all along, please explain (and provide evidence for) the mechanism by which these genes' expression was repressed in so many species for so long, and what these genes are."
One can hope. I do note that Petey just falsified his own pet fantasy (front loading). Poor chap.
"if the genes for bipedality were there all along, please explain (and provide evidence for) the mechanism by which these genes' expression was repressed in so many species for so long, and what these genes are."
I do not misrepresent you, Manning. You simply think in outdated terms of genetics.
The genes for complex traist cannot be located, or named, since it is a network of genetic circuitry that makes such traits. Any systemsbiologist can inform you about this. Thinking in terms of genes is silly and out dates Darwinian talko. If you would know anything about curent biology you should have known this.
Refering to a gene or genes, asking an opponent for upright walking shows that you do not understand biology as it manifest to us today.
Thinking about drifting genes...it encounters the same problem as what the evo-peers here saw immediately as a problem for frontloading: conservation over time.
Selection is the magic word of evolutionism. There is NOTHING else that could potentially be driving the hypothetical proces of microbes turning into man.
@Peer Terborg
Stop wiggling. Answer:
"if the complex traits for certain functions were there all along, please explain (and provide evidence for) the mechanism by which these complex traits expression was repressed in so many species for so long, and what these complex traits are."
PT wrote: "Whole genome duplication hypothesis prior to the evolution of vertebrates, the socalled 2R hypothesis, was falsified over and over by observations on the genomes. Plenty of literature abvailable."
As a botanist, I find polyploidy a familiar and reasonable explanation for many observations. However, animals don't seem as tolerant of polyploidy as plants, so I looked up the "socalled 2R hypothesis."
Turns out the long-running controversy was about whether the whole genome had been duplicated twice in the early evolution of vertebrates, or if only some chunks of chromosomes had been duplicated. Not exactly a controversy that favors frontloading.
In any case, the Wikipedia article on the topic summarizes: 'a more recent review in 2007 by Masanori Kasahara states that there is now "incontrovertible evidence supporting the 2R hypothesis" and that "a long-standing debate on the 2R hypothesis is approaching the end".'
A little further digging led me to a diversity of articles reporting research into the consequences of this ancient polyploidy on vertebrate genomes or into a variety of other closely to distantly related topics. As far as I can tell in a quick overview, the hypothesis looks pretty well accepted at this point.
Peer, By your definition "front loaded" means that all mechanisms and parts of the life system have to be present at once for an organism to function? Am I interpreting you right? Please correct me if I'm wrong
I'm sorry English is your fourth language.
How is this related? I fail to see the connection between Lenski's experiments proving no bacteria can evolve and CE. Are you that blind?
Peer Terborg said: Try frontloaded evolution. It explains it all....and better than the current ideas.
What exactly is it, what does it explain, and how?
I know that explaining things to pest is pointless, but those wishing to understand Allan's point, there is an explanation here.
For plants it is a mechanism of speciation...
For vertebrates is was falsified over and over.
http://www.ncbi.nlm.nih.gov/pubmed/12836688
Of course, a load of people want to revive it...but falsfied remains falsified.
Frontloading is the hypothesis that evolution is an intrinsic property of kinds, which were frontloaded with all information required to vary, adapt and speciate....in other words...to evolve.
Acceptance of hypotheses does not make them true. There is simply no alternative...
No, that would be Behes IC.
Frontloading Frontloading is the hypothesis that evolution is an intrinsic property of kinds, which were frontloaded with all information required to vary, adapt and speciate....in other words...to evolve.
I wrote several papers on it, including many bio-observation that support it.
Manning,
If you do not like my comments here, simply ignore me.
So all the evolution that has ever happened has occurred in ~6000 years (geology and the weak nuclear force I assume being two more "hypotheses" whose acceptance does not make them true in PT's view) due to frontloading that results in tremendously accelerated evolution. In turn, one needs frontloading to explain the fact that we don't observe evolution occurring - oh, wait....
Peer Terborg (real name Peter Borger) is a confirmed YEC as is clear from his use of the term 'kinds'. Peter Borger has written several papers about frontloading (through Variation Inducing Genetic Elements) in the Journal of Creation, but did not adduce biological observations to support it.
Peer Terborg repeats himself, I'll do that too.
Peer Terborg (real name Peter Borger) is a confirmed YEC as is clear from his use of the term 'kinds'. Peter Borger has written several papers about frontloading (through Variation Inducing Genetic Elements) in the Journal of Creation, but did not adduce biological observations to support it.
Not true Peer. It is clearly more rare in vertebrates , but it does happen.
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7998.2011.00829.x/abstract
and as mentioned by others, you should have kept reading after 2003.
http://www.ncbi.nlm.nih.gov/pubmed/25245952
It's a hypothesis; Peter.
I published the hypothesis in 2009, after my papers having been rejected by the secular journals, I chose for the peer-reviewed JoC.
Peter, knowledge on Variation inducing genetic elements and evolution has since then multiplied. Just run a google on TEs and evolution.
TEs are just one of the many VIGEs that reside in the genom to induce heritable and non-heritable variation in genomes. They play importnat roles in all biological processes, incluidng learning.
You missed that? I am not surprised.
I dont know if it only took 6000 years....these are your words.
We know however that the 500 species of Cyclides in the Lake Vicoria took only about 12 thousand years to evolve (it did not contain water during the last ice age). And they make up now an entire ecosystem, alls niches occupied. Evolutionm is not the slow and gradual process theologist Darwin thought it was.
Evolution of wholesome ecosystems from baranomes only takes reshuffling of preexisting info. It is like Lego or a deck of cards.
The other Jim does not even realize that the 2R hypothesis only refers to vertebrates.
Indeed Jim, it does not count for vertebrates. Thanks for confirmation.
And duplication/deletion it is not rare.
The 1000 genomes project demonstrated that huge INDELs explain the difference (which can be 12%) between subpopulations of men
Because you do not read...
"Mikkel, you already started with code."
Nope. Since your foundational premise is wrong, everything else that follows is too.
Only you can correct your propensity to fail.
Then you must have confirmed it, since I never confirmed it myself. I am simply preparing an alternative to the current paradigm. And the frontloading meme is spreading thanks to guys like you. Thanks.
The big surprise of the 1000GP published 2012 was / is that it found 1400 huge indels full of genes making up 12% of the genome.
This confirmed my redundancy hypothesis that I published in JoC 2009.
For the interested:
https://creation.com/images/pdfs/tj/j22_2/j22_2_79-84.pdf
I dont know if it only took 6000 years....these are your words.
Ah - I thought you'd confirmed you were a Young Earth Creationist.
Is it possible in your view that the Earth is ~4.5 billion years old?
But you need selection immediately to conserve those mutations.... Drift no new genes make.
OK, so PT doesn't understand drift, either purposely or through inability.
Why would it be 4.5? why not 4.4? Or 4? Or 3? Or even 1.
You do not know. I do not know.
What I know is that the it does not take millions of years to duplicate or delete genes. Or to reshuffle genomes. That is a matter of generations.
Follow slowly Peer.
1) you claim "For plants it is a mechanism of speciation... For vertebrates is was falsified over and over. ". I think we can assume "it" = whole genome duplications.
2) I then provide a link showing clear, recent examples of WGDs in fish and amphibians. So your statement is false.
3) I then provide a 12+ year more recent paper showing that the 2R hypotheses are still being actively debated. Not actually "solved" back in 2003.
3) You then say genome duplications in vertebrates are not rare, contradicting your comment in 1.
What is your point? Or are you just trolling?
Did Reed Cartwright reply, to Larry's question, or did the question get lost when the creationist p^2's showed up? I am curious to hear the answer as well!
Now it would be surprising if Peter Borger (the name of Peer Terborg) realized how far his ideas are from the scientific literature on TEs.
In plants, polyploidy can, and probably usually does, lead to speciation, but not always. Aside from issues of whether polyploids and diploids should be considered the same species if they look alike, there are some plants that frequently exchange genes between diploids and tetraploids, e.g. Switchgrass. In these, the diploids and tetraploids should clearly be considered a single species.
Of course, the information The Other Jim has provided you about polyploid vertebrates and current debate about the 2R hypothesis are much more relevant to the discussion. (I lived for a while in an area of overlap of diploid and recently evolved tetraploid Gray Tree Frogs.)
Why would it be 4.5? why not 4.4? Or 4? Or 3? Or even 1.
Geology, cosmology, and the weak nuclear force (radioactive decay) are the general answers I can think of off the top of my head.
You do not know. I do not know.
For a definition of "know" acceptable to me (a huge volume of interconfirming consistent data from every type of scientific examination of the question that has been done), yes I do. In your universe, where miracles happen, one can never "know."
PT wrote, "Why would it be 4.5? why not 4.4? Or 4? Or 3? Or even 1. You do not know. I do not know."
Though I'm a biologist, even I know that many rocks contain both unstable isotopes and the daughter isotopes into which they decay. If the amounts of parent and daughter isotopes can be accurately measured, the ratio can be used to determine how old the rock is. The earth must be older than its oldest rocks. When I was in high school, a new "oldest" date was reported about every year. (I vaguely remember 3.65 billion as one of the ages.) Eventually the numbers stabilized and geologists went on to researching other issues.
Why 4.5 billion and not 4 billion? No doubt some geologists could answer, but not me. But I do know why not 1 billion or 3 billion years, and PT can understand that too. Or could if he wanted to.
Hilarious - it is amazing how much unwarranted and naive extrapolation is required to try to prop up creation fantasies.
They never do.
Still waiting for that mechanism that keeps unused alleles whole and usable in genomes for the future.
The problem, Petey, is that the desire to prop up bible fantasies cannot be used as evidence.
Been reading some of "Peer's" comments on other forums from a few years back. In support of his "hypothesis", he once declared, after being shown sequence data exhibiting mutations at 'random' places, that the randomness was so random that it was non-random, and thus supported his claim (this was on the EvC forum). Funny stuff. Funny as in really sad.
No, Pete - you misrepresented me, for I did not write a thing about a single gene.
I do hope you realize that everyone is seeing you as your twist and wriggle out of explaining the actual mechanism behind your creation "science" fantasy.
"if the genes for bipedality were there all along, please explain (and provide evidence for) the mechanism by which these genes' expression was repressed in so many species for so long, and what these genes are."
No answer - only assertions, misrepresentation, and wriggling from the creationist.
So, you have no legitimate answer?
It is all well and good that you want to try to claim that 90% of all "kinds" were the size of a rabbit - but I am pretty sure that no "kinds" of elephants, bison, cattle, etc. were the size of a rabbit. I have seen calculations demonstrating that nearly 2/3 of the ark's volume (and this is NOT including structural supports, decking, etc.) would have been needed JUST for food JUST for the 'elephant kind'. Your unquestioning acceptance of religious myths is nearly as pathetic as your pretense at understanding population genetics and phylogenetics.
Isn't it odd - 'Peer' bio on his 'papers' states:
" He is currently working on the cellular and molecular aspects of pulmonary diseases, such as asthma and COPD, and is an expert on the molecular biology of signal transduction and gene expression"
Yet this EXPERT on gene expression will not even try to explain (meaning that there is no actual evidence) how it is that a front-loaded genome can repress the expression of thousands of alleles over the course of millenia and keep them in working order for when they might be needed in a sub-Kind at some point....
It's Peer reviewed fantasies, though!
Yet this EXPERT on gene expression will not even try to explain (meaning that there is no actual evidence) how it is that a front-loaded genome can repress the expression of thousands of alleles over the course of millenia and keep them in working order for when they might be needed in a sub-Kind at some point....
Apparently the Deity flips that switch when He isn't occupied sticking little outboard motors onto the butt ends of microbes that require them.
Journal of Creation is dedicated to upholding the authority of the 66 books of the Bible, especially in the area of origins. All our editors adhere to the Creation Ministries International (CMI) Statement of Faith and most papers will be designed to support this.
JoC writing guidelines
Amen.
@Larry
"The direct method is not very reliable since the quality of the genome sequences is low and only a faction of the genomes is actually sequenced. Typically about 60-80% of the genome sequence is reliable. The number of potential sequencing errors overwhelms the number of possible mutations so a lot of "adjusting" is necessary in order to weed out false positives and false negatives."
It seems to me this is the take-home message on the discrepancy between the phylogenetic+biochemical, vs direct method.
But why is the direct method so unreliable? I suppose it has something to do with the practical difficulties of sequencing. Wouldn't some effort to try and produce truly accurate sequencing allow us to finally settle the question of the the discrepancy between the two?
But why is the direct method so unreliable? I suppose it has something to do with the practical difficulties of sequencing.
Yes, I saw Reed Cartwright present on this topic a few years back. The signal to noise ratio (i.e. candidate mutations versus actual mutations) is huge--something like 98-99% of candidate mutations are false positives. There are several sources of error. Sequencing is a major one, but somatic mutations are another. The method requires sequencing two adults and a child, each of whom may bear mutations in their body's cellular lineages that create additional uncertainty when trying to establish the de novo germline mutations passed from parents to child. All of these mutations and sequencing errors have to be filtered out with probabilistic models. It's not easy work, and even proportionately small mistakes could lead to reasonably big differences in mutation rate differences.
Except for the usual noise, not a single comment addressing the content.
As modern evolutionism was and is unable to find additional mechanisms to explain info-increase over time, biologists should be encourages to search for explanatory power instead of regurgatating the same old Darwinian canard. If an original though, idea would be spark, this blog would be as dark as night. I have not seen anything here.
Professors, science doctors, come on, we are living in the NGS era. You should have had the evidence for everybody to observe. Please move on beyond the 19th century storytelling which was started by the prophet with the beard. I gave you a handle. Grap it and move on to the next level.
It is fairly easy, Judmarc. It could be TEs, since they are capable of affecting the epigenetic marks downstream of their integration sites. They often function as boundary elements to control the activity of entire genetic landscapes. Furthermore, you can code in more than one frame (which is often observed nowadays in bacteria, but also for regulatory elements in the CEBP genes.
I stopped being active oin the in the internet for a while, because the evo-community is lead b atgheists, who are not interested in adding more complexity to the regulome, the genome in general. They are science stoppers.
I advise everybody to read into this interesting topic of VIGEs. Leave this ignorant blog and delve into the evolution-driving world of VIGEs.
Isn't it funny that the creation scientgists are far ahead of your 19th century selection-thinking. That is because Darwinism (selectionisms) is and always was a science stopper.
Start to think again.
"Leave this ignorant blog": good advise to Peer.
Still no substance, Peter?
It is fairly easy, Judmarc.
It is anything but "easy" if you really think about it. Every alternative you propose calls for some non-evidenced, super-intelligent, super-powerful being to suddenly switch "on" capabilities that have supposedly been "frontloaded" and lying in wait for - how long? (Have you settled on a time frame yet, or are you still uncertain, and if you are uncertain, why exactly is it you feel your uncertainty trumps the mountains of interconnected scientific data available on the point?) And this "requirement" for intelligent direction comes from no direct evidence of same, but simply from your own feeling that surely it must be the case that "mere" stochastic variation, selection, drift, and contingency - all of which we know occur - cannot suffice. Surely a deity must be required.
But none is, any more than something besides blind forces are necessary to create the complexity of a mountain's outline, a river's path, a coastline (hat tip to Slartibartfast for the fjords), or the Earth itself.
The do not have to be switsched on by supernatural power, the switches are transposable and prespecified in the genome and yield instant variation which than only has to spread (through reproduction)
There may even be environmental cues for activation of the right TEs.This has been shown for microbes and plants, and TE activity is regulated and controlled by unknown mechanisms, because nobody is interested in junk...
...but surely there is a whole gene network involved, hundreds of genes.
A recent study in cyclids simply confirms the frontloading hypothesis:
http://www.ncbi.nlm.nih.gov/pubmed/25186727
Abstract•
Introduction•
Accelerated gene evolution•
Gene duplication•
Transposable element insertions alter gene expression•
Divergence of regulatory elements•
Novel microRNAs alter gene expression•
Extensive shared polymorphisms•
Lake Victoria, a recent evolutionary radiation•
Divergent selection on many genes•
Sorting of ancient polymorphisms•
Conclusions•
Accession codes•
References•
Acknowledgements•
Author information•
Extended data figures and tables•
Supplementary information
About 10 thousand years ago the Victoria Lake was dried up.
Now we find 500 "species".
We read: Accelerated gene evolution (multiple alleles doesn't take millions of years to evolve)
We read: huge INDELs and duplications (which make speedy evolution as in the 1000GP)
We read: Transposable element insertions alter gene expression, (because they are VIGEs and not junk).
We read: Divergence of regulatory elements (because no new genes are needed for speciation).
We read: Divergence of regulatory elements (because mutations rates are locally high and most likely directed by environmental cues).
We read: Novel microRNAs alter gene expression (but of course they are not novel...some were just lost from the genome in other species that did not depend on them for reproduction and speciation; Darwinians always mix this up).
This is just one more proof of frontloading which makes speedy evolution.
Time for a novel paradigm.
(Have you settled on a time frame yet, or are you still uncertain, and if you are uncertain, why exactly is it you feel your uncertainty trumps the mountains of interconnected scientific data available on the point?)
It cannot be millions of years because of the redundancy argument I presented above:
https://creation.com/images/pdfs/tj/j22_2/j22_2_79-84.pdf
And because genomic divergence in cyclids also stems from incomplete lineage sorting (ILS) ....this simpy proves independent loss of prespecified genetic elemets.
This whole paper in in complete accord with frontloading, speedy evolution. The evolution of a complete ecosystem in a few thousand years does not require novel genetic information. Man, that is quite something!
Similar observation werd done in the 1000GP projects...
In fact we will observe this in all studies where we include many species and many individuals.
What would be predicted by the mutation converence visitors...
500 fixed species in 10 thousand years?? With a mutational input of 100 SNPs per generation....? Please, give me a break...
Evolution is non-random and VIGE-driven.
Pest: How is this related? I fail to see the connection between Lenski's experiments proving no bacteria can evolve and CE. Are you that blind?
One of us is. Does the name 'Lenski' produce such a knee-jerk reaction in you that you can't think beyond his eponymous Experiment? Here is the very first paragraph, where the distinction is made clear. Its significance is not restricted to lab populations. "It is important to distinguish between the rate at which spontaneous mutations occur and the rate at which genetic changes accumulate in a surviving lineage. The mutation rate reflects the probability of a change in genome sequence between a parent and its offspring. It is the compound result of unrepaired DNA damage, polymerase errors, intragenomic recombination events, movements of transposable elements and other molecular processes that introduce errors during the transmission of genetic information. However, only those mutations in lineages that persist — typically in the face of selection — contribute to the substitution rate that is measured by whole-genome sequencing. The failure to carefully distinguish between these two types of rates is a persistent cause of confusion and misconceptions about whether mutations are random. In the same vein, the frequency of a mutant allele in a population generally does not equal the rate at which the corresponding mutational event occurs."
Do you think people measure mutation rate, or substitution rate, in Cambrian phyla?
Well, where I come from the Bible is considered to have 46 + 27 = 73 books. Any science that doesn't uphold this canon and bow to its supreme authority is heretical, blasphemous and simply wrong. If you start with a fundamentally flawed premise as the cornerstone of your science, how can you get reliable results? You absolutely must reconsider the questions of redundancy, robustness and molecular switches in the light of the indisputable fact that that the Bible has more than 66 books.
Oh so many decades ago (before Bioinformatics was even on the radar) I remember my Professor mentioning the Bible in lecture when referring to
Genesis 7:2
Take with you seven pairs--male and female--of each animal I have approved for eating and for sacrifice, and take one pair of each of the others.
Apparently (and this is the part I found amazing) somebody actually took it upon himself to examine differences in Genetic Variation between kosher and non-kosher animals to prove the point that a literal interpretation of the Bible was indeed correct.
Of course the embarrassing lack of any correlation was never mentioned again.
So sorry for that random act of mischief. ;-)
I am interested in the lack of correlation...can you provide the literature?
Nonsense, deep sequencing long ago solved the problem.
In next-gen sequencing you split up the genome into short segments (what the people I work with settled on are libraries of 250BP, 800BP, 3kBPs and 8kBPs). You then work with an estimated genome size to figure out how many of them you need to get a genome that is as complete as possible. You want to sequence each particular stretch of DNA multiple times, to correct for errors (the number of times you sequence each base is the coverage).
Now what you generally do is to plot a histogram of coverage for k-mers. I.e. you look at the number of times a particular sequence of lenght k turns up in your reads. If you have estimated your genome size correctly, you get a peak at the coverage you wanted, but there's some spread around it. So you want 10x coverage for instance and you get a peak at 10x, but you have some variation around that and some legit reads even only get covered once. At the same time you have error reads giving you another peak at 1 (because most of these errors only occur once), but some of them occur twice or 3 times, etc. If your coverage is high enough these partial distributions only overlap a bit (if you have underestimated your genome size, they might not even show up as distinct - when your coverage is 1x both peaks are at 1...). Now, this means that some novel mutations may land in the region where they might as well be error reads.
You could increase coverage by a lot to make this problem less of an issue, but this means additional expenses and at that point becomes more of a science policy issue. For the price of doubling coverage you could do twice the number of genomes. Is getting a greater accuracy for human mutation rates using this approach (which of course has two alternative estimators) more important than getting a couple of other de novo genomes? I'm in the latter camp - there's more to be gained from increasing the number of taxa for which genomes are available.
In other words, to get the direct method to a degree of accuracy where it would beat the others you would have to invest big money, but you could alternatively sequence a lot of primates to a decent depth, then use phylogenomic approaches to estimate mutation rates per branch (with higher accuracy than the current estimates to boot) and you would be able to resolve quite a bit of the timing of primate evolution on top (and of course such a large scale genomic project would also allow you to look at specific things within the genomes in a phylogenetic context).
It's worth noting that the trends in sequencing are not really about increasing accuracy, but in increasing speed. Next gen sequencing has more errors than Sanger and next-next gen sequencing has more errors than next-gen sequencing. But next gen allows us to sequence hundreds of genomes to at least 80% where Sanger got us one with more effort. And next-next gen will have a similar effect (the ONP comes in USB stick form, you can sequence in the field - well almost at least).
Is it worth trading off accuracy for cheaper and faster genomic data? The answer depends on the research question, but for most of the questions we have right now the answer is yes (it's not that clear for the additional loss in accuracy in NNGS). It's also worth noting that there are diminishing returns here. You spend X money to get to 80% of the genome. To get to 90% you spend 2X, to get to 95% you spend 4X, etc. Most of the interesting bits of the genome are in the 80% - the things that are hardest to get at are things like repeat regions. The question is whether you a prepared to spend as much or more money on finding out how long a stretch of tandem repeats is as you are in finding the complete gene set.
I'm sure you'll be shocked to hear the authors have a different hypothesis than front-loading...
We provide evidence for accumulation of genetic variation under relaxed constraint preceding radiation and involving multiple evolutionary mechanisms, including accelerated evolution of regulatory and coding sequence, increased gene duplication, TE insertions, novel micoRNAs and retention of ancient polymorphisms, possibly including interspecific hybridization.
Amazing how theirs appears to be more in line with modern evolutionary theory.
Of course it is 24 books. ;-)
Contrast Simon and Paul's replies with Peer's as to level of knowledge and detailed factual presentation.
Simon's answer is thorough, but I would add that highly repetitive regions cannot be accurately sequenced with our current technologies (too many ambiguities in the assembly). This apparently only affects genomes with loads of junk, but that pretty much includes all of them. That might be another reason why the direct method is not as reliable as it sounds at first.
Consider the following contention:
Genetic variation was deliberately put in place by the creator in advance, and did not arise from mutation.
Now consider this heartily amusing rebuttal;
…the Ark family had among them at most ten different alleles for each gene locus (3 x 2 = 6 for the wives, plus 2 each for Noah and his wife--their sons would have received all their alleles from their parents). Even if we allow the remote possibility that all three of Noah's sons were adopted and that all eight people on the ark were unrelated, each could have carried only 2 different alleles for each gene locus, and the entire ark family would have 2 x 8 = 16 alleles for each gene locus. So where did all the additional alleles in the modern population come from?
http://paleo.cc/ce/ark-gene.htm
I suppose that would explain why Pat Robertson is begging Ken Ham:
'Let's Be Real, Let's Not Make a Joke of Ourselves'
http://www.christianpost.com/news/pat-robertson-to-ken-ham-lets-be-real-lets-not-make-a-joke-of-ourselves-114063/#ASfyyJtXsTvHxWIH.99
It's a good thing to add. There are some ideas on how the get into HRRs and these mostly involve getting some longer libraries (I think there are now methods that can get >10k libraries), but these of course carry additional costs and the more time efficient assembly strategies use k-mer approaches anyway and therefore you really need to think about how you can utilize these long read libraries to improve the assembly. So that's 2 additional hurdles there.
Thank you both, excellent answers.
"We know however that the 500 species of Cyclides in the Lake Vicoria took only about 12 thousand years to evolve (it did not contain water during the last ice age). And they make up now an entire ecosystem, alls niches occupied. Evolutionm is not the slow and gradual process theologist Darwin thought it was."
But Peer, this is "just microevolution". ROFL.
Hoisted by your own creationist petard.
Peer: 500 species of Cyclides in the Lake Vicoria...
Please... these are cyclides, and these are cichlids.
@Peer Terborg
The "frontloading hypothesis" makes as much sense as saying:
"See there is an alphabet of 26 letters, all the information contained in Shakespeare's writing was there all along ! Proof: Shakespeare did not invent a single letter".
======================================================
@all
I slowly but surely understand why "Peer Terborg" is so afraid of being exposed a Peter Borg.
The degree of incompetence, arrogance and cowardice he displays would, if publicly known, make collaborators, 'grant-givers' and sane students run away from him.
So he sticks with his personal type of "lying for Jesus!"
______________________________________________________________
We are still waiting for for him to answer a few questions posed to him (his desperate wiggling & hand waving attempts don't count for answers).
Among others:
1. N. Manning asked:
"Still waiting for that mechanism that keeps unused alleles whole and usable in genomes for the future."
2. In the previous post he admired "Gnomon" for his "brilliant, establishment-shaking" papers without understanding that (their value aside) these papers are actually ad odds with his "frontloading-nonsense". He failed to answer how he reconciles his admiration for "Gnomons" work with the fact that "Gnomon" is basing his analysis (keeping it's value and relevance aside) on rather classical evolutionary thinking.
______________________________________________________________
In his attempt to spam the entire thread he comes up with ever new references to papers allegedly supporting his B.S. without ever explaining how this actually supports his views.
==Even more funny: In full Gish-Gallop he does not even recognize that he is permanently contradicting himself, for example talking to Mikkel Rumraket Rasmussen he says:
"Mikkel, you already started with code. Code is only stabilized when it is essential to the reproduction of an organisms. That is what you call selection. Selection is merely conservation of preexisting code. Now I ask for new code without selection and you say mutation. But you need selection immediately to conserve those mutations, and that can only be done if they positively affects repruduction. So mutation is not the mechanism. Mutation is the variation of Darwin which can be selected. A mutations may also drift for a while, but for an complexity increase selection is required. Drift no new genes make. "
==In a later 'contribution' he cites a paper on cichlid evolution:
"Abstract•
Introduction•
Accelerated gene evolution•
Gene duplication•........"
...without recognizing that Gene duplication followed by later mutation caused divergence in sequence (and function) is a classical example how new information can be acquired by a genome.
Al,
This is all BS and I hope you realize that. You can't prove any of that. Why would you expect me to believe it? No one knows what the cause of cambrain expolisivo was. Why do you insist on making me believe you?
Some time try figuring out how many colleges Oxford University has.
Pest, I don't know how on earth you can read these distinctions between mutation rate and substitution rate - real, mathematically definable characteristics of any process of descent with mutation - and think I was saying something directly supportive of any particular theory on the causes of the Cambrian explosion.
I was talking about the distinction between mutation rate and substitution rate. If you don't know the difference, and you won't be told the difference, then discussion on your original point - "how do scientists estimate the mutation rate" - is pointless. You're not worth bothering with, in short. Have fun.
Peer says:"Nonsense, deep sequencing long ago solved the problem."
Right. So, the multi-step validation process undertaken by Cartwright et al. (2012) to classify mutations from their trios into four categories, only one of which is the desired de novo germline mutation category (and which comprises only ~1.5% of candidate mutations) was actually redundant because "deep sequencing long ago solved the problem". You should totally do a comment in Nature on that.
Kia ora Paul
I dug up an old reference that had me gob-stopped back in 2012:
http://www.livescience.com/21709-individual-sperm-genomes-sequenced-for-first-time.html
First consideration - these results were obtained by what was then called a revolutionary new technology called "Single Cell Sequencing"
They were able to sequence the genetic makeup of single cells, such as cancer cells, but this is the first time anyone has determined genome sequences for individual spermatozoa as compared to the original progenitor somatic cell sequence.
Second consideration - 91 individual spermatazoa from a 40-year-old man with a healthy semen sample who already had normal children were analyzed.
Results: They found that recombination occurred 23 times, on average, in his sperm cells. The rate of recombination and genetic mutation varied widely between spermatazoa. They identified between 25 and 36 single-nucleotide mutations in each sperm cell.
Back in 2012: I said "WOW!" then "YIKES!"
Reading your post above now makes me wonder about the likelihood of "false positives".
Peer Terborg said Evolution is non-random...
Funny you should mention that; Darwin said it already 160 yers ago.
Yeah, but not because of selection...as you believe.
Why should I consider such contension, which not even advocated by any well informed bioscientist.
I asked for literature and you provide an internet assay by glen kuban, who doet not even show up in pubmed.
And a newspaper....
Please provide standard peer-reviewed literature to back up your claims or just leave the arena. 'Let's Be Real, Do Not Make a Joke of Yourselve'
The other Jim,
Okay I follow slowly. The problem is you just link and do not explain. The first linked shows recent polyploidity in amphibians. It is a nice and instant mechanism for diversiviation.
THe second link assumes that the 2R hypothesis is true and confirms it using only one genefamily of 8 members. That is nice, but most families do not confirm the 2R hypothesis, rather falsify it. As shown in my previous link.
Of course, you are free to believe in events that never happened.
Tell me, what is the use of confirming a falisified hypothesis? The 2014 paper you linked is merely more noise disturbing the signal.
Of course I know the use of confirmative science (which does not bring anything): you want to have it true, because there is no alternative.
So, in fact, it does not matter what we observe. It is true anyway.
Again: The 2R hypothesis was already falsified in 2003:
J Struct Funct Genomics. 2003;3(1-4):85-93.
2R or not 2R: testing hypotheses of genome duplication in early vertebrates.
Hughes AL1, Friedman R.
The widely popular hypothesis that there were two rounds of genome duplication by polyploidization early in vertebrate history (the 2R hypothesis) has been difficult to test until recently. Among the lines of evidence adduced in support of this hypothesis are relative genome size, relative gene number, and the existence of genomic regions putatively duplicated during polyploidization. The availability of sequence for a substantial portion of the human genome makes possible the first rigorous tests of this hypothesis. Comparison of gene family size in the human genome and in invertebrate genomes shows no evidence of a 4:1 ratio between vertebrates and invertebrates. Furthermore, explicit phylogenetic tests for the topology expected from two rounds of polyploidization have revealed alternative topologies in a substantial majority of human gene families. Likewise, phylogenetic analyses have shown that putatively duplicated genomic regions often include genes duplicated at widely different times over the evolution of life. The 2R hypothesis thus can be decisively rejected. Rather, current evidence favors a model of genome evolution in which tandem duplication, whether of genomic segments or of individual genes, predominates.
Of course; I could confirm that the earth is green, but, as a scienctist, I prefer falsifications.
Wilson: "Though I'm a biologist, even I know that many rocks contain both unstable isotopes and the daughter isotopes into which they decay.
Yeah, bu you do NOT know the original situation. How many assumption do you think there are to date a rock?
No, I am not surprised since is was discussed from the selection paradigm...and as you know selection can be negative, positive, strong, week, sweepy, etc...like the good old 16th century phlogiston.
You mean, rocks may have been created last Thursday with isotope ratios meant to fool us into believing they were hundreds of millions years old? And I suppose outer space was filled with photons heading for the Earth and pretending they came from distant stars? And dead trees were created with carefully crafted fake growth rings to fool dendrochronologists? And the whole Universe is one big hoax?
Mikkel,
Why would this be microevolution? Within a few millenia 500 species, a complete ecosystem appeared from one probably one original uncommitted genome. It is superfast. This is exactly what a creation scientist would like to have. And it is real.
I do not see any observable evidence for Darwinian gradualism. This is only assumed. The real biological data in the African Rift lakes demonstrate that no long ages are required.
Probably the same counts for the marsupial fauna in Australia. Genetics indeed show that all marsupials are grouping and probaly descented from one uncommited genome (baranome).
@ Peer
I cannot recall the details of a negative result casually made in passing over 30 years ago. My apologies.
I do have one question for you
Given
a gene locus in the human leukocyte antigen complex has 59 different alleles (Ayala et al, 1993). However, each individual person [including each of the 10 people on Noah's Ark] normally has only two alleles for a given gene locus (one allele from each parent)
Can you please explain the origin of human leukocyte antigen complex's other 41 different alleles?
No one needs to be a well informed Bioscientist to appreciate the impossibility of YEC.
Until you can come up with a reasonable explanation for all this genetic variation since clearly front-end loading is no longer an option, I think your welcome on this forum has been long exhausted.
Paul, as a matter of fact, I ran NGS project finding the TE-regulated transcriptome in asthma genes, and we sequened with a coverage of >30. So, all our sequecnes were 100% reliable.
I am interested in completele describing and understanding the human genome, not in as many as genomes as can be possibly sequenced (with low coverage).
There is a mechanism for generating mutations in the genes for the HLA system, Tom. One mechanism involves TEs.
Given that the human population went through a bottle around 100 thousand years ago, a genome of 3x10^9, and a random mutaion rate of 0.5 x 10^-9 mutations per base-pair per year, we cannot exacpe the conclusion that a non-random mechanims is at work to drive variation in specific parts in the genome, particularly the genes involved in the immune system (MHC genes, TCR genes, IG genes).
Peer Terborg (real name Peter Borger) wrote:
“Paul, as a matter of fact, I ran NGS project finding the TE-regulated transcriptome in asthma genes, and we sequened with a coverage of >30. So, all our sequecnes were 100% reliable.”
No report of this research has appeared, only a letter with P. Borger as corresponding author announcing this work.
Nicola Miglino, Michael Roth, Florent Baty, Martin Brutsche, Michael Tamm and Pieter Borger, 2012. Asthma and the regulated retrotransposon transcriptome. European Respiratory Journal 40: 788-790 doi: 10.1183/09031936.00189811 0 times cited
“Peer Terborg Sunday, April 26, 2015 11:23:00 AM
Please refer to me as Peer. I need this pseudonym for safetz reasons. Otherwise I have to stop posting here
Peer Terborg Sunday, April 26, 2015 11:34:00 AM
We all know I am PB, but for safetz I would like not to have my pseudoname exposed”
Does this mean Peter Borger’s employers don’t like his YEC activities? They can scarcely be ignorant of them. Or does Peter Borger want to continue to spout on internet despite being warned to lay off?
OK - Peer fell into the trap.
Would others more qualified than I please do the honors of finishing him off.
It would appear that Peer is now in fact advocating rear-end loading - both literally and metaphorically.
;-)
Peer: Paul, as a matter of fact, I ran NGS project finding the TE-regulated transcriptome in asthma genes, and we sequened with a coverage of >30. So, all our sequecnes were 100% reliable.
I am interested in completele describing and understanding the human genome, not in as many as genomes as can be possibly sequenced (with low coverage).
Maybe this 'Peer Terborg' account is just a bot that randomly replies without understanding of the content of thread at hand? Otherwise, if Peer Terborg was a person who had run NGS projects, they would understand that they would need to deal with the *actual* statistical properties of the problem at hand, and not simply say that 30x coverage = 100% accuracy. They would also understand that sequencing errors and somatic mutations are not the same thing. Otherwise, frankly, not so different from @horse_ebooks.
You know what I mean. If I was just following your mainstream opinions, you would applauded...
We deepsequenced 12 genes and their surrounding with a >30 coverage (most genes even >100 coverage) and we did not have to doubt our data.
I wish you good luck withyour low coverage genomes (which will not bring anthying new, just a waste of money and time).
Pathetic Peter likes to reiterate my name....
I will spell itz out for you P-E-T-E-R_B-O-R-G-E-R
I am sure you will never forget me. For the rest of your life I have occupied a spot in your brain....
Why would it be a trap...
Everyday new alleles arise in the soma of B and T cells by mutational-mechanims. I can imagine that something similar is going on in the germline of HLA genes. For sure there was extended recobination between HLA genes in the HLA locus, so why do you exclude additional variation-inducing mechanisms?
Tell me? Is it because of preconcived ideas about evolution? Dogma? Belief? Worldview?
we did not have to doubt our data
Just that right there should make any thinking person doubt whatever you have to say.
Ah - you mean that the data actually fits the current paradigm, so your statement that "A recent study in cyclids[sic] simply confirms the frontloading hypothesis:" is actually not true. A creationist playing fast and loose with the facts, quote mining and misrepresenting data. I'm shocked.
As an aside, even 16th century phlogiston is still 4700+ years more up to date than the creationism you are trying to sell. ;-)
The joke is of course that you fight your own nonsensical conjecture that not a single ID or creation bioscientist advocates.
"Genetic variation was deliberately put in place by the creator in advance, and did not arise from mutation."
Of course it arose from mutations. The question is: are they introduced purely at random or by a non-random DNA sequence-dependent mechanism. The latter we observe for the immune-system genes, TCR, BCR and MHC.
Please... professors and doctors in evolutionary philosophy, teach this old peer, who read about it 30y BP, some 21st century molecular biology. :-)
You know what I mean...you can simply not stand that I do not advocate and support the meanstream nonsense on evolution.
That is the whole point...as soon as you start to dount the premises and conclusion of the "expert evolutionst" you have to weigh your words...
This is what happens when a creed is introduced to science.
It would appear some present need to be brought up to speed on 19th Century Bioscience.
Just to be clear here - Am I correct in understanding that you no longer propose a Young Earth Creation? In other words you have retreated from the notion that was Noah's family survived the flood close to 4,400 years ago, roughly 1,650 years after the creation?
Where did I propose this? Can you point that out for me.
As far as I know, I have never proposed this. I appears that you are only able to fight your own conjectures.
I am not interested in dating the earth, dating the flood or whatever. I do not even know whether one would be able to date such things, without preconcetiuons and assumptions.
I am solely interested in biology..
Really?
So in your opinion, how long has the human lineage existed?
How long has life in general on this planet existed?
How old is the planet?
I have a passing curiosity what your answers to these questions would be... given previous answers attributed to you would change the direction of this exchange entirely. Unless, of course you have changed your mind.
My opinion is that I do not know. I am trying to find out by studying biology from a non-preconceivbed framework. I studies both ID, creation and evolution scenarios...and found them all wanting.
That's why I started to rethink and rewrite biology. The only scientists that are open and appreciate change are those in the ID/creation camp. Not the selectionists, evolutionists with their Darwinian and other dogmata.
weasel
stop wasting everybody else's time
as soon as you start to doubt the premises and conclusion of the "expert evolutionist" you have to weigh your words...
This is what happens when a creed is introduced to science.
You always have to weigh your words and doubt your data and conclusions. That is not what happens when a creed is introduced to science, that is science, at least the good careful kind.
It cannot be millions of years because of the redundancy argument I presented above:
https://creation.com/images/pdfs/tj/j22_2/j22_2_79-84.pdf
You not only contradict yourself (when you said previously that you didn't know how old the Earth was, it might be 4 billion years, 3, 2, 1...), you throw out cross-confirming data from many independent branches of science on the basis of a bunch of careless nonsense (i.e., your article) that conflates randomly duplication, redundancy, and junk DNA.
What you are doing isn't serious study, it is making enough of a mess that you can see anything you imagine in it, like a Rorschach blot.
"There are those who interpret the data differently" is not the same as "falsified". Clear yet?
Peter Borger is covering his tracks on the internet. The article “Evidence for the design of life: part 1—genetic redundancy” in Journal of Creation 22(2) 79-84 had Peter Borger as author. See http://evoinfo.org/papers/auxilary/borger1.pdf . This is the original 2008 version.
However, the identical article “Evidence for the design of life: part 1—genetic redundancy” on Creation.com http://creation.com/genetic-redundancy gives Peer Terborg as author. Note that on this page the link to Journal of Creation leads to a contents page listing Peer Terborg as author. The Journal of Creation must have altered its content pages.
Peter Borger’s employers must dislike his YEC activities. Peter Borger must have been warned to lay off.
"Peer" said,
"What I know from my asthma studies is that evolution is never required to understand the data."
Exactly the point you idiot. You are blind to what evolution might tell about your data because you have no idea about evolution other than your fantasies. Just like you have non idea about the age of the planet other than your fantasies.
"Peer" said,
"To stabilize frontloaded information for eons is impossible and therefore the eons have never existed."
Of course. "Peer" proposes "frontloading" to try and fit biology into his religious fantasies, and then uses the same "frontloading" stupidity to confirm that the eons are wrong, as his religious fantasies indicate. No kidding "Peer"!
"Peer" asked,
What I am really interested in is the whether modern evolutionists have come up with anything in addition to selection that can explain an increase of genomic information, which must have taken place from microbe to man evolution.
Of course. Those interested could look at "The origins of genome architecture" and articles by Michael Lynch (Indiana University). But you Peer, you would be unable to understand it. It requires some proper understanding of evolutionary theory, population genetics, and other concepts which might be too hard for your misinformed and malformed intellect.
Hey P-E-T-E-R_B-O-R-G-E-R aka Peer Terborg,
You say that the genes for upright walking are rather genes in a morphengenetic regulatory network, but we do not know all individual members.
Would it be correct to assume that you do not think that entire set of human genes are involved in this "morphengenetic regulatory network" but but rather a proper subset of them ?
Given that then would it be correct to assume that this subset could in principle identified at which point a "reductionary" approach is possible ?
Otherwise one would have to assume that you think that all human genes are involved in each and every identifiable aspect of the human phenotype, which would be just plain crazy.
I mean that would be a theory of sorts, but it would have very little, as in no, explanatory power, would it ?
Peer, what photosynthesis is saying is that unless you are married to the evolutionary theory as he is, you will not "believe" in the "proper understanding of evolutionary theory"- something Larry couldn't have said better. In other words Peer, you are doomed because you ask too many unanswerable questions and just like quest you will be eventually banned .
Steve I think, we all know you are a moron. Don't broadcast it for Darwin's insane....
I keep hoping a creationist or IDist will say something original or striking, something I have to think about.
That has happened several times and caused me to look stuff up or pay close attention to the conversation. So far, nothing on this site has met that criterion. The only time Peter or Peer enters my consciousness is for the few moments i spend realizing I need to use the scroll wheel. A week away from this site and all memory of this encounter will be gone.
But Peer Terborg is god's trooper, surely god doesn't allow Peer to make any mistakes. After all, Peer and his work is infallible. In a way, when Peer does any work it's god's own work so is assured to be without error or subject to doubt. Actually in some way, Peer is god.
Pest,
It's not an issue of believing, but of understanding. Since Peer doesn't understand evolutionary theory, since his "background" in evolutionary theory consists on creation "science" fantasies, he's bound to be unable to understand the answers to the questions he pretends to ask.
I am not married to any theory you idiot. Stop projecting your deficiencies onto others. Since you can't think beyond your religious fantasies you think that we're the same. We're not.
There is no Peter Borger on the JoC website, Peter.
Go to another playground for your kindergarten level contributions.
Denisovan, there's a typo
Thanks. I fixed the one typo.
Larry,
Interesting post.
(a) In paragraph 5 you say “Given that the human genome is 3.2 × 109 bp…”. In paragraph 15 you say “The human genome consists of 6.4 × 109 base pairs (6.4 billion).”. I think you mean the haploid genome in paragraph 5 and the diploid in paragraph 15.
(b) In paragraph 11 you say “…the quality of the genome sequences is low and only a faction of the genomes is actually sequenced.” Do you mean *faction* or *fraction*?
(c) I am having a very hard time understanding the Units of Measure you are employing at various points in this post. For instance, I am getting confused between births and cell divisions. You are describing a *rate*, but what units is it expressed in? I also need to see a calculation laid out. E.g.,
E = Number of base pairs in egg
S = Number of base pairs in sperm
Z = Number of base pairs in a somatic cell of the zygote resulting from E + S
Zd = Number of base pairs in a somatic cell of the zygote zygote that are different from corresponding base pairs in E and S
Mutation Rate = Zd / (E +S) [Units = base pairs per individual per generation]
Thanks!
Thanks for spotting the typos. I corrected them.
There are several different kinds of mutation rate. The three that I talk about are the rate per bp, the rate per cell division, and the overall rate per generation.
There are roughly 100 new mutations per generation. I prefer to use a mutation rate of 100 per generation for humans.
If you want to convert this to base pairs then it's roughly 1.6 × 10^-8 per base pair per generation.
Late to the discussion by a couple years. "New" genetic information can occur in many ways. An example is the yeast genome duplication event, discussed here http://dx.doi.org/10.1371/journal.pbio.1002221 .
How does a large genome duplication contribute new genetic information?
A rare duplication of a large chunk of the genome that contains one or more highly advantageous genes for a given environment can drastically increase the fitness of that individual. With this large duplication, a large number of other genes are duplicated that were already near their optimal expression patterns, and thus their duplication likely decreases the fitness of the individual moderately.
The enormous advantage for the environment of the small number of genes that were duplicated creates a new fitness landscape. Rapid selection for mutations that alter the function or reduce expression of the bystander duplicated genes can be inferred from the sequence information we have today (as in brewing yeast). A subset of the duplicated genes were repurposed for specialized tasks, and many were mutated so that they are no longer expressed.
Another source of novel genetic information include viruses. Though there are thousands of papers that could be referenced, an interesting one can be found here: http://dx.doi.org/10.1371/journal.pgen.1003122 . Giant viruses seem to have acquired DNA elements from eukaryotes and bacteria and combined them to produce fit virus particles. The extremely high mutation rate and extraordinary selection pressure on viral populations repurpose genes taken from other species. These viral populations are incubators of novel genetic information through high mutation rates, gigantic numbers of progeny, and high selection for fitness. A good example is HIV, which actively keeps its genome mutation rate high (doi: 10.1089/AID.2013.0153).
It is not difficult to see how a novel gene function spawned from a virus can be transferred back into a new host, especially since many clades of viruses actively integrate their information into the host genome! How many times have you gotten a viral infection? Any one of those viral particles may have inserted some foreign DNA into the genomes of some of your cells.
There are dozens, if not hundreds, of relatively common occurrences that can introduce new genetic information. The "frontloading" hypothesis only makes sense if you ignore the pieces of data that don't fit a preconceived hypothesis.
So there are about 1-2 amino acid changes per generation? And perhaps .1-1 changes in regulatory DNA?
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