Strolling with a skeptical biochemist
Is it the Lenski experiment?
It's the number of generations since Noah for 'evolution in Kind' of organisms with a generation time of 3 weeks.
What would a biology lab have to do with evolutionary biology?? Perhaps its a contract thing for asking a raise in salary.
What would a biology lab have to do with evolutionary biology??Blink. By running an experiment on it, perchance?
Hey Robert,By way of analogy, what would an xtian church have to do with morality??But that's a bad analogy because churches don't actually have anything to do with morality (except as an example of how to do it wrong).
I feel like the fact that I work in that lab would give me an unfair advantage in answering...
Cool! I had no idea.
No of generations in LTEE?
This post looks like it's going nowhere so let me put the cat among the pigeons:"experimental techniques in microbial evolution have advanced to the point where the fate of a novel mutant strain within a controlled population can be followed over many generations. Thus, these experiments are on the verge of being able to test our theoretical predictions of the fixation probability—,predictions that have in many cases stood untested for 80 or 90 years. This is extremely exciting."The fixation probability of beneficial mutationsZ. Patwa and L. M. Wahl J. R. Soc. Interface (2008) 5, 1279–1289So has Linski or anyone actually tested the predicted fixation prob for a beneficial mutation? Does anyone know?
Richard Lenski answers questions about the long-term evolution experiment (LTEE)On the unpredictability of evolution and potentiation in Lenski's long-term evolution experimentHow do creationists interpret Lenski's long-term evolution experiment?Lenski's long-term evolution experiment: the evolution of bacteria that can use citrate as a carbon sourceEvolution in Action and Michael Behe's ReactionElizabeth Pennisi writes about Richard Lenski's long-term evolution experiment
I think he deserves a Nobel.Yes, really.
lets see 63`000 generations of bacteria...12 cultures....50 ml per culture....10^9 organisms per ml culture .... makes 10^9 x 50 x 12 x 63.10^3= 37.8 x 10^12 = almost 40 trillion organisms. And he found three mutations in pre-existing biological pathways?How does this translate to humans? Trillions of Austalopithecuses on the African planes produced the HAR1F gene? The FOXP2?Lenksi indeed deserves the Nobel.... For falsifiying evolution.
Does anyone still wonder why I call them IDiots?
There's many many more than three you dolt. Where the hell do you get this number from? Look at this graph from one of Lenski's papers:There are hundreds. After 40.000 generations more than 600 mutations have accumulated in the genome. Notice how the carrier slowly crawls higher and higher in relative fitness. That means those mutations are beneficial mutations too.
Being off by only 2 orders of magnitude is pretty remarkable for a creationist if you ask me. haha.
Mikkel,Improved fitness is evo-obscurantism and means nothing but increased reproduction rate. The organisms gained a reproductive adavantage (due to loss of regulatory elements) of about 70%. Most of the regulatory genetic changes and losses were due to insterion sequences (IS).Evolution of this type is frontloaded and predominantly determined by IS elements. Transposons (TEs) have a similar function in eukaryota. They are mistakenly interpreted as virus-remnants but in fact they are variation-inducing genetic elements. Variation is frontloaded. Evolution is a process frontloaded in the genomes of all life. These VIGEs are the basis to understand the origin of RNA viruses.
almost 40 trillion organismsHave you noticed that there's a bottleneck in the experimental protocol?
Peer, what defecating bodily orifice did you extract the numer three from?
Allan,Yep, from the endstage culture 1 ml (= 1 billion organisms) is taken and diluted 1:50. Because the cultures are contineously mixed, the genotypes of all previous generations will be present in the next round of selection. Lenski excellently designed the experiment.
"Improved fitness is evo-obscurantism and means nothing but increased reproduction rate."Actually by calling it evo-obscurantism you are engaging in an attempt at minimizing the strength of the evidence with silly rethorical devices. Fitness is defined as reproductive rate, that's what it means. This was never obscured by the word fitness. "The organisms gained a reproductive adavantage (due to loss of regulatory elements)"Making shit up again are we? Peer Terborg, the IDiot liar, lying for his religious beliefs.
"Because the cultures are contineously mixed, the genotypes of all previous generations will be present in the next round of selection."That's not what 1:50 means you dolt. Only 2% of the total genetic diversity of the flask makes it to the next one. Here's a hint that the diversity is random and not "mixed": Only one lineage evolved the ability to grow on citrate under aerobic condition. Peer, it really helps if you aren't completely clueless.
Lenski reported that his evolved organisms gained a reproductive advantage of 70% relative to his original organism. He also reported that most of the adaptive fenotypes were related to insertion sequences. Further, I am not religeous. Beliefs I have, surely, like you.Why do you lie about the similarity of chimp and man genomes? I could call you a liar, but I feel that you do not deserve it. You are most likely ignorant about it.
Yep, from the endstage culture 1 ml (= 1 billion organisms) is taken and diluted 1:50. So you realise you can't just count every cell in every flask ever? Or, if you can, you should count all the somatic cells in those Australopithecines, or every gamete.
Further, I am not religeous. Beliefs I have, surely, like you.Like us? No way, LOL. Borger, stop projecting your delusion and at least be honest to yourself. You're certainly not fooling anyone here buddy
Yes, I wonder, Larry Sandwalk. So, why don't you start explain, instead of speaking your usual insults.I really wonder how the Lenski experiment could inform us about human genetic changes to explain HAR1F and FOXP2. Or don't you know what these genes mean for humans? I guess you don't know. Let me explain: HARF1F requires 18 specific mutations compared to chimp. FOXP2 needs 2. With only 600 mutations in 40 trillion organisms (the number of organisms that Lenski used in his experiments), evolution is going nowhere on the African planes.Eevolution is just a joke.
What could Larry Sandwalk's reponse be other than "IDiot"?
Hey Borger, so are you assuming that the mutation rate is the same in mammals? And also, what about genome size?How come humans are OBSERVED to be born with some 100 mutations in average?
evolution is going nowhere on the African planes.Tee hee.
Mikkel,have you ever thought about your 600 mutation and 40`000 generations in a human perspective?40'000 human generations translate to about half a million years, taking 15 years as the generation time. From Australopith to now that adds up to 5000-6000 mutations in human reproducing cells. It all boils down to frontloading. For both IDiots and Darwimps it is the only way out.
Peer, the average human is born with over 100 mutations. Our genome is much bigger than the measly ~4 megabase genome of E coli. By almost three orders of magnitude. 40.000 human generations would add up to 4 million mutations if every generation has 100 new ones. Supposing the same is true for chimps, and supposing as you write, that 40.000 generations translate to about half a million years, that means if humans and chimps split from their common ancestor about 6 million years ago, they'd have accumulated each about 48 million mutations. That gives 96 million mutations total difference between them. How different would that imply they should be genetics wise if they shared a common ancestor 6 million years ago? Let's see: 96 million / 3.2 billion *100 = 3% difference (or 97% similar). What does the human and chimp genome projects estimate the degree of genetic similarity between chimps and humans to be? Oh, about 97%. You evolved, get over it.
I understand what you want to say. The first problem is that the genomes of chimp and man are not 3% different, but at least 8% (the part of the sequences omitted from the studies because they did not align). Further, the DNA sequences of human subpopulation already differ by 10% according to the 1000 genomes projects. There must be something wrong.
"There must be something wrong."There is definitely something wrong. Fortunately, stupidity is curable. But first you (Peer Terborg) have to admit that you have a problem.
"Further, the DNA sequences of human subpopulation already differ by 10% according to the 1000 genomes projects. There must be something wrong."I realize that you're getting into to Gish-gallop territory here, so I should not even bother asking, but I would like to see the citation for this claim.I'd be willing to buy the notion that 10% of sites in the human genome are variable among different subpopulations. However, any two individuals drawn from a random sample will likely differ in much less than 10% of their sites.
Yes, I admit I have a problem...I admit I had my math wrong, although that should not be a big deal, here.Your problem is the HAR1F and FOXP2...I am still waiting.
And more gish gallop! Goalposts keep moving! Classic.No Borger, it's not that you got your math wrong, you got all your assumptions wrong, you proved that you have no clue what you're talking about.
Dave Carlson,look up the publications of the 1000 genomes projects consortium. They were published in 2007, 2010 and 2012 in Nature. As a matter of fact, the difference between humans was 12% due to indel (as I predicted on my weblog 2006 because variation is generated by indel mutations through actions of TEs). I published summaries of my "krank" ideas in the JoC. You can also read them there. Most "evolution" is just unselectable variation due to VIGEs. And because universal common descent has also been proven wrong beyond any doubt, this blog is just about nothing.It is all frontloaded.
Yes, Dazz, I admit I had several things wrong...Instead of 63'000 generations of 50 billion, there are now effectively 63'000 of 1 billion. Good to know. That really helps, isn't it.
Peer,I looked at the two most recent (2010 and 2012) 1000 Genomes Project Nature publications and could not confirm your 12% claim, but for the sake of the argument let's say that's it's true. How precisely is this a problem for evolution? Please be specific.
Peer Terborg says,As a matter of fact, the difference between humans was 12% due to indel (as I predicted on my weblog 2006 because variation is generated by indel mutations through actions of TEs). From "Global variation in copy number in the human genome" Nature 444:444-454 doi: 10.1038/nature05329A total of 1,447 copy number variable regions (CNVRs), which can encompass overlapping or adjacent gains or losses, covering 360 megabases (12% of the genome) were identified in these populations.A total of 265 people were analyzed for the presence of duplicated regions of the genome and deletions. The average size of the deletions/insertions is about 300 kb (0.01% of the genome). A follow-up study in 2010 found 8,599 validated CNVs with a total coverage of 112.7 Mb or 3.7% of the genome. The reduction in total coverage of the deletions and insertions is due to increased resolution of the breakpoints. (Conrad et al., 2010 Nature 464:704-712 doi: 10.1038/natureo85160. Conrad et al state that, on average, a pair of individuals differs by 24 Mb or 0.78% of the genome length. The 1000 Genomes Project looked at CNVs in 179 individuals (Mills et al., 2011 Nature 470:59-65 doi: /10.1038/nature09708). They identified many more CNVs because they were able to look at very small deletions and insertions. They found 28,025 CNVs with a median size of 729 bp and an average size of 8 kb. The total coverage comes to 224 Mb or 7.0% of the genome. As with previous studies, no two individuals differ by anywhere near this amount.
What could Larry Sandwalk's reponse be other than "IDiot"?It could be worse, all letters lowercase.
The latest paper on insertions and deletions (CNVs or SVs) identifies 202,000 variant regions with an average insertion/deletion of 10 kb. This means that 63% of the human genome is subject to changes in copy number. It does not mean that there are two humans whose genomes differ by 63%. MacDonald et al. (2014) Nucl. Acid Res. 42:D986-D992 doi: 10.1093/nar/gkt958
Whether or not there are two humans whose genomes differ by 7 or 12 or 63% is not the point. The point is that human sequences can vary up to 7 or 12 or 63%. It is highly redundant. Genomes are plastic entities subject to self-induced, VIGE mediated changes. The result is indels and very fast diverging genomes. This is where variation has its origin. Variation is due to frontloaded mechanism driven by VIGEs. Point mutations hardly play a role. The chance-driven mechanism proposed by the NeoDarwinians is folly. That is why I discussed this in the Lenski thread with his 63 trillion organism. You can never translate this type of evolution to man and other slowly reproducing organisms. Maybe Larry, or Mikkel, can tell us how long it would take for the HAR1F to evolve in a Darwinian world.Mutational input: 100 / generationEstimated max. population size: 10.000Required specific mutations: 18 (to form and stabilize a small regulatory loop in the preexisting primate HAR1F homologue gene)The HAR1F is an RNA-coding regulator gene, monomorf in primates, but with 18 differences in man.Please, be my guest.
Cut the crap with the HAR1F Borger. Evolution isn't teleological, remember? It didn't have to be the HAR1F, calculating the probability of an event after the fact doesn't tell you anything about the probability of some event happening. Actually, after the fact, the probability is 1. It happened, so there's a 100% chances the it happened.
*that it happened*
Just remember, Peer, every time you read someone won a lottery at odds of hundreds of millions to one: your math is wrong.Here's a straightforward math problem for you: Calculate the chances you - specifically you - were born as the child of your parents - specifically your parents - who were born specifically as the children of their parents, etc., etc., back through the generations to the first humans on earth (you can calculate that date as 6K years ago if you like, I don't really care). In other words, what are the odds you came to exist in exactly the way you in fact did? I think you'll finds odds are overwhelming that you aren't really here (which is different than not being all there).
Dazz, in mammals mutations rates are very much slower relative to bacteria.The whole concept of random accumation of genetic noise as the engine for evolution is just bogus. The genomes of all studied organisms contain specifically designed mechanims to induce variations in offspring. It is this variation we observe in organisms and of which Darwin thought the origin was unknown and thus "random". But we now know what it is. Everyone knows about it, but it is still not recognized as such, because of the simplistic Darwinian 19th century attitude towards genomes and how they function. A huge part of the genomes exist of (the remnants of) variation-inducing genetic elements.
Borger, you idiot. Read Mikkel's post above. You just assumed you could extrapolate the figures in Lenski's experiment to mammals and you are dead wrong. It's so stupid that it boggles the mind
What are the implications of an E. coli mutation rate on the order of 10^-10 mutations/bp/replication ? Given a genome size of 5×10^6, this mutation rate leads to about one mutation per 1000 generations anywhere throughout the genomeIn humans, a mutation rate of about 10^-8 mutations/bp/generation (BNID 105813) was inferred from projects where both parents and their children were sequenced at high coveragehttp://book.bionumbers.org/what-is-the-mutation-rate-during-genome-replication/
oops. One spot...
Yes, and as said, and I realize now that I did not take the genome size into account. Thanks for pointing it out, you brilliant one. So, we now have 63'000 generations of 1 billion effective organisms per generations...yeah that is quite a lot. 63 trillion. More than three times the debt of the USA in dollars. So, in 63 trillion organisms random evolution was able to adjust three pre-existing metabolic pathways. Really great.Now for HAR1F and FOXP2.
Under stringent selection, that is...the end of evolution as we know it.
Conclusion: the only way out is a non-random mutational mechanism. Frontloading. Crank but true.
Is the frontloading mechanism of evolution at work in the Lenski experiments? How would you detect it?
"How would you detect it?"Prayer?
"was able to adjust three pre-existing metabolic pathways. "Where do you get this number from?
Surely this evolved from his earlier uttering (near top of the page) "And he found three mutations in pre-existing biological pathways?"But I guess he just likes that number: https://en.wikipedia.org/wiki/3_(number)#In_religion
Peer,your book was published in 2009, we're now 6 years in the future. As a scientist you know that the only way to validate your ideas is in the lab. Negative attacks in the 'X we see today, it's too complex to have evolved, thus it must have been designed, thus goddidit' doesn't count as evidence as you should know as scientist.In the 6 years since the book, you must have applied to Dutch grant organizations to get funding for your idea. Perhaps even gone to European grant organizations? How many grant proposals did you actually write? How many got funded? And what was the overall consensus of the review commentary on your proposals, the ones which didn't get funded?I know from experience grant organizations can be a nasty lot to deal with, they're funding gets cut each year and only award grants to really worthwhile proposals. A proposal which would set the current scientific consensus on evolution on it's head, should grab tonnes of money in no time.
Ed, that is a lovely set of questions :-)PS: as 'Peer' has not been based in the Netherlands for a while, he could not apply to Dutch grant organizations after publishing his book (in Dutch only, so no use for grant applications anyway).
In the Lenski experiments, the IS driven evolutionary mechanism dominated the adaptive fenotypes. lenksi even reported on that in an early phase of his work.The socalled citrate bacterium is a fluke, the edge of evolution, that can only be established in huge populations of bacteria and viruses. It can simply never function to prove human evolution.That is what you guys do not want to understand, but is clear to anyone dealing with human or primate genes and genetics.Look at any of the human accelerated regions (HARs). You cannot explain them using Lenski's experiments and insights, because they are only valis in superfast reproducers. That's why I challenge you all with the human HAR1F.
To Ed: As a scientist I am aware of the fact that extraordinary claims require extraordinary evidence. I do not claim that "X is too complex, it cannot have evolved". On the contrary. I say, genetic changes are due to a mechanism present (frontloadedd) in the genomes and evolution does not have to wait for helpful mutations to arise at random or by chance. I also say, selection does not play a dominant role in evolutionary processes. And I say, modern biology has falsified the Darwinian hypotheses (universal common descent, gradualism and selectionism) over and over. I say: evolution is frontloaded and mediated. Life has more than one origin. That's all I say. I realize this is utter against the Darwinian consensus, but not against science and not against the observations.That Darwinism persist is solely a matter of pushing, propaganda and the absence of an naturalistic alternative.
But now there is a naturalistic alternative. It is frontloaded evolution. Bio-information was frontloaded. Evolution is nothing but a reshuffling of this information. The role of natural selection is finetuning the preexisting genetic programs. Frontloaded evolution is science. It explains why the major part of the genome can be indel-ed. It explains why genetic redundancy is not associated with duplications. It explains neutral evolution and why selection is such a weak biological force only involved in processes directly related to reproduction.
Peer,you forget to answer my questions, let me remind you. It's 6 years since your book came out, how many grant proposals have you written to get funding for you claims? Of the proposals you sent in, how many have been funded? How many experiments have you performed to provide evidence for your claims? Since you claim "Frontloaded evolution is science." it means experiments can be performed.I'd be interested to know, which experiments can you perform to prove this? And how.
Three replies from 'Peer Terborg', none of which even attempts to answer Ed's question. Instead, just the usual creationist blurb.I think 'Peer Terborg' simply won't answer Ed's question, which is not a particularly hard one: just some fact finding.
Hi Peter BorgerI decided to look up the hyper accelerated region you've been alluding to (p.s. The clue is in the name as to what happened here)This article mentioned that the sequence in question which contained the 18 SNPs (between humans and chimps) was 118bp long which helped me to track it down.Here is the alignmentI went looking for this sequence because I was interested to see how it would compare in Neanderthals. It just so turns out that they have sequenced roughly half of this 118bp region in Neanderthals. There are 52 nucleotides in the Neanderthal sequence and in this short subsequence, we already find 3 mutations separating neanderthals from modern humans!Here is the alignment including Neanderthals. None of these three mutations group neanderthals back with chimpanzees - they appear to have been later mutations that have arisen in the 800,000 years separating neanderthals from modern humans.Now I'd like to ask you a question... If 3 mutations can appear in a subset of this sequence that is just under half the length and if this can take place in a mere 500k - 800k years then why should we have trouble believing that this region could undergo 18 mutations over a period estimated to be 10 times as long (5 - 8 million years)?Your argument from incredulity fails disastrously when we consider the accelerated changes that have happened in Neanderthals as well!
Even more fun - go and look and the SNPs for the HAR1F region (Chr 20 (NC_000020.11):63.10M - 63.10M);http://www.ncbi.nlm.nih.gov/variation/view/Within humans the region has 67 copy number variants and;Exon 1 - 128 SNPs, 14 deletions and 20 insertion (this exon is 1963bp)Exon 2 - 59 SNPs, 1 deletion, and 2 insertions (this exon is 831bp)Intron - 68 SNPs, 2 deletions (300bp, so it has 3.4x the SNP rate). So unlike the claims at the ID/creationist links that Peer got this locus name from, it is not just a magic jump to a one, special human sequence, then sitting there happily.
Ed, Missed your question. I handed in three grants (two to the ERC, one to the SNF) to study the regulatory/evolutionary functions of TEs in the development of complex diseases. One was granted. I am in the final stage of analysing my data.
AceofSpades,apperently you are not aware of the pitfalls of retrieving and mending Neandertal DNA (it undergoes a series of chemical treatments). So, I doubt the 3 mutations are due to random mutational processes. Then, you assume 800 thousand years.Further, you assume evolution and extrapolate from it using several unwarranted assumption. This is merely question begging.I do not assume anything. In reality, we (I did it myself using NGS) have measured the mutational input (100 / generation) and we know the number of mutations in the HAR sequence. That is all we need to show that the HAR regions cannot be the result of a random accumulation of mutations. I prefer to do science, with real data, which are free from assumptions. Your question begging above is not science.
In my opinion, it is very unscientific, even stupid, to deny that mutations may be the resulst of a mechanism, similar to what we observe in the generation of T cell receptors or the B-cell antibody germline.If I put a plasmid in the genome of a bacteria, I can predict with great certainty were the mutations will occur.There are mechanisms present in the genome that facilitate mutations. Of course, I understand the phylosofical implications for such determinism. But I face them, rather than to ignore or deny them.
"Frontloaded evolution is science" - Peer Terborg many times.Ed asked: "which experiments can you perform to prove this?"The experiments Peer Terborg refers have to be part of the Schweizerischer Nationalfonds 2010 grant to professor Tamm, with three cooperators, Peter Borger amongst them:"Die Suche nach regulatorischen Retrotransposon-Transcriptome in komplexen Erkrankungen: Am Model des Asthma""The search for the regulatory retrotransposon-transcriptome in complex diseases: the case of asthma. "I'm not sure what this might mean: that asthma was frontloaded?
"Even more fun - go and look and the SNPs for the HAR1F region (Chr 20 (NC_000020.11):63.10M - 63.10M);http://www.ncbi.nlm.nih.gov/variation/view/"Loads of LOL, indeed. Go and have look here:http://omim.org/entry/610556We are talking about an RNA gene with regulatory function. Previously coined junk DNA by the Darwinians, it is full of regulatory RNAs. The genome is an RNA computer with protein output.
One article has Peter Borger as co-author and mentions transposable elements:Asthma and the regulated retrotransposon transcriptome By: Miglino, Nicola; Roth, Michael; Baty, Florent; et al.EUROPEAN RESPIRATORY JOURNAL Volume: 40 Issue: 3 Pages: 788-790 Published: SEP 2012 0 citationsNothing about frontloading in that: not even universe wide.The article gives a sketch of planned experiments.
In reality, we (I did it myself using NGS) have measured the mutational input (100 / generation) and we know the number of mutations in the HAR sequence.Fortunately for us, other people not as dogmatic as you have looked into these things and realizing that the whole genome does not have the exact same mutation rate.http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.0020168Your favorite end-region of Chromosome 20 is specifically mentioned...
Well Peter BorgerThis is just really embarrassing for you. You've been presented with evidence that HAR1F has mutated quickly in Neanderthals as well and instead of considering the evidence, you've looked around desperately for any reason to brush it aside. Instead of presenting a reasoned response or looking into whether you might be wrong, you've revealed your biases. I think it's obvious to everyone here now that you're so desperate for evolution to be refuted that you will desperately grapple around for any unsubstantiated reason to brush evidence that challenges your world view. In your desperation to justify whatever it is you want to believe, you've been blinded by confirmation bias.Here is the sequence in question showing the 3 mutations and ALL of them have an excellent quality score of 40.Not only that, but there is another sequence read (also of high quality) which overlaps with this one and it confirms one of these three mutations. So now you've been caught with your pants around your ankles. The evidence clearly shows that HAR1F has also mutated quickly in Neanderthals independently of modern humans yet you dogmatically stick to your views, brushing aside anything that challenges your simplistic view of the world.What it seems to me we are seeing here is a particular sequence that has become highly prone to mutations. A faster mutation rate in this particular region explains perfectly why Neanderthals are also gathering lots of independent mutations in the same region. I'm willing to bet that if we were to consider a number of modern day humans we would see an assortment of new mutations here as well.As The Other Jim has said, there are regions within our genome that mutate at faster rates than others.
My first thought was "something to do with a number of populations?" but then, thinking of your over-the-top militant atheist propaganda, I made a mistake and decided that it has to with a number of scientists signing something that supports evolution (or something along these lines). My bad. Lenski's experiment is brilliant.
That's what I mean. Believing Lenski's experiments are brilliant means you do not understand mutations, genetics and evolution of slow reproducers.Therefore, once more I refer to the HARs in men. Larry -- or Mikkel -- please show how long it would take to evolve the human HAR1F gene from the primate sequence, using the known mutational input (100/generation), the commonly accepted effective population size (10000) and selective coefficient (lets assume any point mutation in HAR is mildly beneficial = 1% increased fitness). You will find out that Lenski's experiment is useless for Darwinians studying slow reproducers.
Is there evid3ence of frontloading in the Lenski experiments? What evolutionary innovations did it produce?What is your hypothesis for how the HAR1F gene evoloved, and what evidence do you have to support it?
Not only that but what's the evidence that the HAR1F sequence even has a biological function? References, please.
I'm not a biologist, nor even a scientist, but it seems obvious that accumulated point mutations are not the only, or even the best, explanation for observed large differences in genes between closely related lineages. The Wikipedia article on HAR genes pointed me to another article on gene conversion, which seems a more plausible mechanism.https://en.wikipedia.org/wiki/Gene_conversion
Here, we see that Larry Moran does not even understand his own babypet neutral evolution. Prof Larry, de HAR1F accumulated mutations far beyond neutrality.Further: http://omim.org/entry/610556So, start doing your calculations please. I did them already. Let's see where you go wrong.
J.Chapman,I know what gene conversion is. Can you point out how gene conversion (of pre-existing genes) introduces 18 point mutations?It all boils down to: evolution cannot explain origin questions. It is pretending to address origins, but all real bio-data scream: frontloading. All mechanisms evologists involve to "explain" biology always imply frontloading. It is not going to be better.
Crhris: "Is there evid3ence of frontloading in the Lenski experiments? What evolutionary innovations did it produce?"Lenski in 2004: "This review shows that IS elements are useful as markers for detecting genomic change over experimental time scales and, moreover, that IS elements generate some of the beneficial mutations that increase organismal fitness."http://myxo.css.msu.edu/lenski/pdf/2004,%20Res%20Microbiol,%20Schneider%20%26%20Lenski.pdf
IS elements are the bacterial counterpart of transposons, transposable and transposed elements in eukaryota.Evolvability, adaptation, generation of variation is a built-in trait of all organisms.
That means that Peter Borger interpretes any and all TE IS or whatever that generates mutations as evidence of frontloading.Now he has to show that mutations are directed even if generated by IS or TE. But perhaps 'generated' already means frontloaded to Peer Terborg/ Peter Borger. and again about that SNF grant: what is frontloaded about asthma?
In fact, you do not even have to direct them (although many have been demosntrated to be sequence or site-specific). The point I want to make is that there are mechanisms in the genome that generate variation in the offspring. Most observed variation is mediated by such mechanism, hence NeoDarwinian hocuspocus can finally be dropped. It was dead in the water from the start and its only contribution to biology was scientific DELAY (remember Mendel, McClintock, junk DNA, etc).Darwinism is and was and always will be a science stopper. Its dogmas are anti-science. Apart from that it is a dangerous philosophy. Promoting Darwinism as fact is criminal.
"and again about that SNF grant: what is frontloaded about asthma? "Not asthma is frontloaded, the mechanisms that regulate gene expression and which is disturbed in asthma, were frontloaded. The genes, the control and regultory elements (TEs), they are all frontloaded. We found that 30% of the human genes initiated from TEs. We performed an exact screening for TEs in asthma-associated genes and determined copynumber variation as well as mutations affection regultory processes. It is the way to understand complex diseases, variation and death through senescence.
"The point I want to make is that there are mechanisms in the genome that generate variation in the offspring. "Mechanisms like transposition and not 100% repair? Things that have been known from before you were born? What a discovery have you made!What you would have to show for frontloading is that these mutations are favourable: increase fitness. Or don't you understand what frontloading means?" to direct them (although many have been demosntrated to be sequence or site-specific)." So you don't know what directed mutation means?Now explain the connection between frontloading and asthma.
Wha would I explain your misinterpretation? I said, the TE-associated mechanims that regulate gene expression are frontloaded. Not asthma. Asthma is not frontloaded. Asthma is (hypothetical) due to genes that are deregulated through uncontrolled accumulation of TEs in the wrong place. Degeneracy is a logical consequence of defunct TE-activity. That's all.You may tell me Why asthma was frontloaded...
(some crossposting)Comment to Peer TerborgTuesday, September 29, 2015 10:17:00 AMIn that explanation "frontloading" is an empty word, signifying nothing. "We found that 30% of the human genes initiated from TEs. We performed an exact screening for TEs in asthma-associated genes and determined copynumber variation as well as mutations affection regultory processes. It is the way to understand complex diseases, variation and death through senescence." That makes sense. ".... the mechanisms that regulate gene expression and which is disturbed in asthma, were frontloaded. The genes, the control and regultory elements (TEs), they are all frontloaded. " does not add anything to the explanation. What DO you mean by "frontloading"?
And btw...we already know that you know that I am Peter Borger. But I would like you to also refer to me as Peer. Is that to much for you?
"Asthma is (hypothetical) due to genes that are deregulated through uncontrolled accumulation of TEs in the wrong place. Degeneracy is a logical consequence of defunct TE-activity" Quite possible, not problem. "TE-associated mechanims that regulate gene expression are frontloaded"That is a totally superfluous sentence without any explanatory value. What DO you mean by 'frontloaded'?
Frontloading: all elements required for evolution were present from the start. Evolution is nothing but reshuffling and/or duplication of preexisting DNA elements regulated by TEs which are also alreayd present from the start and only expand or contract due to indels. No new information required for evolution.
O yes, almost forgot...frontloading reduces natural selection and point mutations to what they really are: insignificant.
10:31:00 AMThis explanation about frontloading has nothing whatsoever to do with the explanations about TEs and asthma:"We found ....... and death through senescence." makes sense."Asthma is (.......TE -activity" Quite possible, no problem.No relation with evolution. An explanation about frontloading that has no empirical content whatsoever."TE-associated mechanims that regulate gene expression are frontloaded" is pure and undiluted belief, not substantiated by anything.
The SNF grant was to study the regulatory/evolutionary functions of TEs in the development of complex diseases. Good. That is, the grant did not address frontloading and the explanation about the results makes sense - until one gets to frontloading. it is impossible to address "all elements required for evolution were present from the start" from a tudy on asthma gene regulation. That is Peter Borger can publish quite nice thank you results about asthma gene regulation and TEs, whereas Peer Terborg has no data and only unsubstantiated opinions his alter ego has no evidence for.
Nice summary, Peter.Always reminds me of http://www.noanswersingenesis.org.au/realsnelling.htm ...
I am aware of Lenski's IS work from the 90's. What I asked was in the ongoing E. coli experiment that produced citrate metabolism, where are the frontloading evolutionary developments, and how do you detect them?In a separate question, how is HAR1F evolution an example of frontloading?
@eelco That's hilarious!Is Dr. Andrew Snelling competing with Jeff Thompkins for the position of world's greatest creationist troll?
Dr Borger and Mr Terborg?
I would suggest Poor Retord For Dr. Borger's next moniker.
Peter, and all the others...you folly around and don't even understand that evolution and the development( evolution) of diseases is the same.LOL!
Chris B: "I am aware of Lenski's IS work from the 90's. What I asked was in the ongoing E. coli experiment that produced citrate metabolism, where are the frontloading evolutionary developments, and how do you detect them?"Citrate metabolism a new trait?....please give me a break. Try to get a copy from a biochemistry book and look up citrate metabolism. Citrate is the most important intermediate in the TCC...try a google for citric acid cycle.Othing new was added to the genome in Lenskis epxerpiment. You are being fooled by the Darwians, who believe that one can select metabolism from scratch. Folly!
How do you propose that citrate metabolism suddenly appeared in E. coli, where it had previously been absent?
"Citrate metabolism a new trait?....please give me a break. Try to get a copy from a biochemistry book and look up citrate metabolism. Citrate is the most important intermediate in the TCC...try a google for citric acid cycle.Othing new was added to the genome in Lenskis epxerpiment. You are being fooled by the Darwians, who believe that one can select metabolism from scratch. Folly!"Translation: I can't answer your questions. Here are some troll insults instead.No one, except you, said that citrate metabolism evolved de novo in Lenski's experiment. One lineage evolved the ability to utilize citrate under aerobic conditions. This happened when a citrate transporter protein was duplicated and the extra copy was co-opted to transport citrate under the aerobic conditions of the experiment. No frontloading there.With regard to IS elements, Lenski's review paper that you quotemined earlier in this thread also showed quite clearly that the increases in fitness in E. coli over the long term experiment decelerated over time, while the movement and shuffling of IS elements continued unabated, leaving the role of IS elements in increasing fitness rather vague. Of course, the many deleterious mutations caused by IS elements, well-documented in the literature, will simply die off undetected in this experiment. So what is your hypothesis on the IS elements? Are they directed in some way (other than the already established facts of target insertion sequences, etc.?In a separate question, how is HAR1F evolution an example of frontloading?
Btw, DK, I am not an over the top creationist...I am a realistic biologist, who simply goes where the data lead me. Selection had never anything to do with evolution, the putative process transforming bacteria into bacteriologists. It is merely finetuning pre-existing genetic information.
Let us play "What is your logical fallacy!"https://yourlogicalfallacyis.com/personal-incredulityBut I have to give your credit for composting the fallacy twice, in both directions, in that second sentence!https://en.wikipedia.org/wiki/Argument_from_ignorance#Argument_from_incredulity.2FLack_of_imagination
"Btw, DK, I am not an over the top creationist...I am a realistic biologist"Of course you are. And orangutans are purple. And stars are little cubicles with fluffy pink clouds.
For me, a realistic but color blind biologist, orangutans are brown, and stars are yellowish spots in the night sky. For you, Eelco, they may look like fluffy pink clouds. But you are the cosologist, who I am not going to oppose.Anyway, biological systems as we observe them on earth are frontloaded-with-information entities. That is what I deduce as a biologist.
Slow progress - the word 'realistic' has disappeared in the last sentence.
Can't handle some well-deserved mockery ?
Can you explain why I would deserve it?No opposition allowed in the Darwinian world?
You manage to make such an utter fool of yourself here (and elsewhere), that as an expression of gratitude and admiration you receive some well-deserved mockery. Congratiulations ! Keep up the good work of making a fool of yourself, and you will get some more mockery for your efforts. Fair enough !
Peer TerborgThursday, October 01, 2015 10:16:00 AMIf doubting the role for mutation-selection in some well-defined biological puzzles (like the HARs or the SRGAPs) is the same as making a fool of oneself, than we know for sure that this weblog is not about science. Good science needs doubt. Bad science only needs dogma.In biology, in good science, we work with hypotheses and null-hypotheses. In biology, the null-hypotheis for the hypothesis mutation-selection-did-it is ID. When the hypothesis fails, the null-hypothesis gains strong support. The genome is strong support for the null hypothesis.Apparently, it is not done to perform experiments or calculations that show the hypothesis is wrong and that support the null-hypothesis. Is there a third way? I doubt it.
'Peer': "If doubting the role for mutation-selection in some well-defined biological puzzles (like the HARs or the SRGAPs) is the same as making a fool of oneself, ..."If, indeed, because doubting stuff is NOT how you are making a fool of yourself. You clearly don't get it ..."In biology, the null-hypotheis for the hypothesis mutation-selection-did-it is ID."That sort of nonsense is how you make a fool of yourself, not doubting stuff.