The “We share 99% of our DNA with chimps” claim rises again

I am not sure if anyone has brought this up before but I was watching at documentary on Neanderthals and it occurred to me: Why do scientist say 96% of human DNA is the same as chimp DNA, but only 1-2% of human DNA is the same as Neanderthal, and 50% of our DNA is the same as our parents and siblings? That is a rhetorical question, I know the answer. But I think it is relevant to point out that scientists use statistics to subliminally influence how people think. https://news.nationalgeographic.com/news/2005/08/0831_050831_chimp_genes.html Chimps, Humans 96 Percent the Same, Gene Study Finds https://www.livescience.com/42056-neanderthal-woman-genome-sequenced.html They estimated about 1.5 to 2.1 percent of DNA of people outside Africa are Neanderthal in origin http://genetics.thetech.org/ask/ask138 We share 1/2 of our genetic material with our mother and 1/2 with our father. We also share 1/2 of our DNA, on average, with our brothers and sisters. The documentary on Neanderthals is here: https://www.youtube.com/watch?v=6hIyD1QlX9k Jim Smith

No Darwinist is willing to prove me wrong? What happened to your faith in Darwin? The 99% identical genome of humans and chimps just kills Darwinism and you know it. Find another mechanism if you can. In the mean time I'm going to sequence my and my younger brother's genome. He is a closet Darwinist. Can anybody predict the results of our genome sequencing? How close can we be? KevNick

Seversky: You are of course free not to reply to people when they respond to you. I would not put a gun to your head to force you to converse. At the same time, if you make a claim, and someone raises objections, and you don't respond to the objections, your critic can be said to have won by default, since you have abandoned the defense of your claim. I will therefore treat all my unanswered objections to your claims as decisive refutations until such time as you respond. So right now it's Timaeus 5, Seversky 0. And of course, others here, whose responses to you have also gone unanswered, may have accumulated even higher totals. Timaeus

Timaeus So that you won’t feel ignored: Timaeus @ 29

I agree with Barry above that you have missed the article’s point. You seem to be reading too quickly. And that is not surprising. You seem to comment on column after column here, but never stay long on any one column long enough to have a sustained, back-and-forth discussion with anyone, a discussion where points and arguments are exchanged and people on both sides modify their views.

And what both you and Barry seemed to have missed is that I was commenting on what I thought were pertinent points in the comments posted under the News byline in the OP.

Your approach, for the most part, is scattershot. You toss in a drive-by comment, then move on to the next column which catches your interest, toss in another drive-by comment, move on again, etc. Most people who respond to you don’t get even a single reply to their responses. It’s as if you have what teachers for the past few years have been calling “ADD” — attention deficit disorder — and are unable to stay long at any one task, being too easily distracted by background activity in your environment.

I, like you, will post in any way that I see fit or not post at all, as the case may be. There are reasons why I’m not able to post with the frequency or at the length of some others here. When I do post, I have no expectation that anyone will necessarily answer and I’m not offended by a lack of comment. No one is obliged to answer or to read my comments at all. Seversky

Thank you for your illuminating posts, bornagain77. Seems like a "Copernican" revolution in genetics is starting to gain momentum. While browsing around, I found some interesting statements in the following paper, first about the 1% difference, and later about brain size. http://genome.cshlp.org/content/15/12/1746.full For example

Also, what might seem an important phenotypic difference between humans and great apes might not actually be the most critical factor in determining unique features of the human condition. For example, despite the frequent attention given to big brain size (Wood and Collard 1999; Preuss 2005), there is little evidence for causative connections between brain size and human cognitive abilities (Preuss 2005).

Then, I found it curious in one of wd400's responses that the chimpanzee genome is actually larger (about 7% larger) than the human genome. It seems likely that it would be difficult to reconcile that 7%, which does not exist in the human genome, with the 1-2% reported difference between the genomes. At any rate, it seems to be a non-issue, and I suppose it's further evidence of the limited role of DNA in distinguishing the species. But not everyone agrees. It also brings to mind the hilarious New York Supreme Court Justice Barbara Jaffe, who briefly granted chimpanzees the same legal protection as humans regarding detention. I wonder what's next? Quotas for university admissions? Having the right to vote? Driver's licences? Another hearing on May 6 should reveal what Judge Jaffe has discovered! ;-) -Q Querius

Genetic breakthrough that reveals the differences between humans - 2006 Excerpt: The findings mean that instead of humanity being 99.9 per cent identical, as previously believed, we are at least 10 times more different between one another than once thought (99%) - which could explain why some people are prone to serious diseases. http://www.independent.co.uk/news/science/genetic-breakthrough-that-reveals-the-differences-between-humans-425432.html Marching to our own sequence: Study finds DNA replication timing varies among people - Nov 13, 2014 Excerpt: A new study from geneticists at Harvard Medical School and the Broad Institute of Harvard and MIT has found that this replication plan—including where the origin points are and in what order DNA segments get copied—varies from person to person. The study also identifies the first genetic variants that orchestrate replication timing. "Everyone's cells have a plan for copying the genome. The idea that we don't all have the same plan is surprising and interesting," said Steven McCarroll, assistant professor of genetics at HMS, director of genetics for the Stanley Center for Psychiatric Research at the Broad and senior author of the paper. "It's a new form of variation in people no one had expected," said first author Amnon Koren, postdoctoral fellow at HMS and the Broad. "That's very exciting." http://phys.org/news/2014-11-sequence-dna-replication-varies-people.html New level of genetic diversity in human RNA sequences uncovered – May 2011 Excerpt: A detailed comparison of DNA and RNA in human cells has uncovered a surprising number of cases where the corresponding sequences are not, as has long been assumed, identical. The RNA-DNA differences generate proteins that do not precisely match the genes that encode them.,,, Nearly half of the RDDs uncovered in the new study cannot be explained by the activity of deaminase enzymes, however, indicating that unknown processes must be modifying the RNA sequence, either during or after transcription. ,,, Although all of the individuals analyzed in the study had a large number of RDDs, there was a great deal of variability in the specific RDDs found in each person's genetic material." http://www.physorg.com/news/2011-05-genetic-diversity-human-rna-sequences.html

Genomic Mosaicism is another semi-related finding that also contradicts what Darwinism would have predicted

Ask an Embryologist: Genomic Mosaicism - Jonathan Wells - February 23, 2015 Excerpt: humans have a "few thousand" different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,, The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It's called genomic mosaicism. In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,, ,,,(then) "genomic equivalence" -- the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA -- became the accepted view. I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common. I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It's the organism controlling the DNA, not the DNA controlling the organism. http://www.evolutionnews.org/2015/02/ask_an_embryolo093851.html

Of supplemental note to post 104

Why the 'Gene' Concept Holds Back Evolutionary Thinking - James Shapiro - 11/30/2012 Excerpt: The Century of the Gene. In a 1948 Scientific American article, soon-to-be Nobel Laureate George Beadle wrote: "genes are the basic units of all living things.",,, This notion of the genome as a collection of discrete gene units prevailed when the neo-Darwinian "Modern Synthesis" emerged in the pre-DNA 1940s. Some prominent theorists even proposed that evolution could be defined simply as a change over time in the frequencies of different gene forms in a population.,,, The basic issue is that molecular genetics has made it impossible to provide a consistent, or even useful, definition of the term "gene." In March 2009, I attended a workshop at the Santa Fe Institute entitled "Complexity of the Gene Concept." Although we had a lot of smart people around the table, we failed as a group to agree on a clear meaning for the term. The modern concept of the genome has no basic units. It has literally become "systems all the way down." There are piecemeal coding sequences, expression signals, splicing signals, regulatory signals, epigenetic formatting signals, and many other "DNA elements" (to use the neutral ENCODE terminology) that participate in the multiple functions involved in genome expression, replication, transmission, repair and evolution.,,, Conventional thinkers may claim that molecular data only add details to a well-established evolutionary paradigm. But the diehard defenders of orthodoxy in evolutionary biology are grievously mistaken in their stubbornness. DNA and molecular genetics have brought us to a fundamentally new conceptual understanding of genomes, how they are organized and how they function. http://www.huffingtonpost.com/james-a-shapiro/why-the-gene-concept-hold_b_2207245.html

bornagain77

It's about 1000 USD to sequence a genome (wholesale). Two humans picked at random will be about 99.9% identical on average. wd400

unwilling participant, What happened to mutations and natural selection? Are you telling me that environment drives the inconceivable changes in body parts by regulating gene expressions? Really. I hope you have a mechanism for this process and more than pure Darwinian speculation. New blueprints out of nowhere? Please surprise me. I'm all ears. KevNick

How much does it cost today to sequence a human genome? I'm pretty sure that if we were to sequence my genome and any of the Darwinists on this thread, our genomes wouldn't be even 97% identical. I love bets and I may have a sponsor to cover the costs of the genome sequencing. Would anybody like to challenge me? KevNick

wd400 as to: "The rest of your post reveals we appear to have a different meaning of the word “gene” in mind. I meant the simplest one, a unit of inheritance."

Landscape of transcription in human cells – Sept. 6, 2012 Excerpt: Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.,,, Isoform expression by a gene does not follow a minimalistic expression strategy, resulting in a tendency for genes to express many isoforms simultaneously, with a plateau at about 10–12 expressed isoforms per gene per cell line. http://www.nature.com/nature/journal/v489/n7414/full/nature11233.html Time to Redefine the Concept of a Gene? - Sept. 10, 2012 Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins! While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25. Based on these results, it seems clear that the RNA transcripts are the real carriers of genetic information. This is why some members of the ENCODE team are arguing that an RNA transcript, not a gene, should be considered the fundamental unit of inheritance. http://networkedblogs.com/BYdo8 Duality in the human genome - Nov. 28, 2014 Excerpt: The gene, as we imagined it, exists only in exceptional cases. "We need to fundamentally rethink the view of genes that every schoolchild has learned since Gregor Mendel's time. Moreover, the conventional view of individual mutations is no longer adequate. Instead, we have to consider the two gene forms and their combination of variants,",,, "Our investigations at the protein level have shown that 96 percent of all genes have at least 5 to 20 different protein forms.,,, http://medicalxpress.com/news/2014-11-duality-human-genome.html Multiple haplotype-resolved genomes reveal population patterns of gene and protein diplotypes - 26 November 2014 Excerpt Discussion: Our global view of haplotype/diplotype diversity in relation to population size suggests that current efforts are still far from capturing the majority of gene forms and that saturation may not even be achievable. The concept of a predominant, ‘wild-type’ form of ‘the’ gene appears obsolete for over 85% of genes, challenging traditional ‘Mendelian’ views. This highlights the need for an expansion of current concepts of ‘the’ gene^29, along with the development of appropriate documentation and language. The enormous diversity of haploid and diploid gene forms raises fundamental questions concerning the relationships between sequence(s), structure(s) and function(s)^21 http://www.nature.com/ncomms/2014/141126/ncomms6569/full/ncomms6569.html

Towards the latter half of the following podcast, Dr Sternberg, who has a PhD in evolutionary biology, elucidates how the overturning/loss of the ‘gene’ as the central unit of inheritance turns the modern synthesis of neo-Darwinism from a science into no better than the discarded alchemy of yesteryear.

Podcast – Richard Sternberg PhD – On Human Origins: Is Our Genome Full of Junk DNA? Part 5 (emphasis on ENCODE and the loss of the term ‘gene’ as a accurate description in biology and how that loss undermines the modern synthesis of neo-Darwinism) http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-5/ The Extreme Complexity Of Genes - Dr. Raymond G. Bohlin https://vimeo.com/106012299 Design In DNA – Alternative Splicing, Duons, and Dual coding genes – video (5:05 minute mark) http://www.youtube.com/watch?v=Bm67oXKtH3s#t=305

bornagain77

Sequencing and assembling genomes is hard, no one in their right ming would think it was the best way to estimate genome size. We know from flow cytometry that the chimp and human genomes are about the same size, the current build of the chimp genome is actually a little longer than the human one The rest of your post reveals we appear to have a different meaning of the word "gene" in mind. I meant the simplest one, a unit of inheritance. I guess you meant just protein coding genes or some other restrictive definition. wd400

here are some supplemental comments/quips as to neutral theory:

Majestic Ascent: Berlinski on Darwin on Trial - David Berlinski - November 2011 Excerpt: The publication in 1983 of Motoo Kimura's The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura's theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. "A critique of neo-Darwinism," the Dutch biologist Gert Korthof boasted, "can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science." By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian. http://www.evolutionnews.org/2011/11/berlinski_on_darwin_on_trial053171.html

With the adoption of the 'neutral theory' of evolution by prominent Darwinists, and the casting under the bus of Natural Selection as a major player in evolution, William J Murray quips,,,

"One wonders what would have become of evolution had Darwin originally claimed that it was simply the accumulation of random, neutral variations that generated all of the deeply complex, organized, interdependent structures we find in biology? Would we even know his name today? What exactly is Darwin really famous for now? Advancing a really popular, disproven idea (of Natural Selection), along the lines of Luminiferous Aether? Without the erroneous but powerful meme of “survival of the fittest” to act as an opiate for the Victorian intelligentsia and as a rationale for 20th century fascism, how might history have proceeded under the influence of the less vitriolic maxim, “Survival of the Happenstance”?" - William J Murray https://uncommondescent.com/intelligent-design/why-keith-blanchard-really-doesnt-understand-evolution/#comment-510124 Ann Gauger on genetic drift - August 2012 Excerpt: The idea that evolution is driven by drift has led to a way of retrospectively estimating past genetic lineages. Called coalescent theory, it is based on one very simple assumption — that the vast majority of mutations are neutral and have no effect on an organism’s survival. (For a review go here.) According to this theory, actual genetic history is presumed not to matter. Our genomes are full of randomly accumulating neutral changes. When generating a genealogy for those changes, their order of appearance doesn’t matter. Trees can be drawn and mutations assigned to them without regard to an evolutionary sequence of genotypes, since genotypes don’t matter. https://uncommondescent.com/evolution/ann-gauger-on-genetic-drift/ Here is a Completely Different Way of Doing Science - Cornelius Hunter PhD. - April 2012 Excerpt: But how then could evolution proceed if mutations were just neutral? The idea was that neutral mutations would accrue until finally an earthquake, comet, volcano or some such would cause a major environmental shift which suddenly could make use of all those neutral mutations. Suddenly, those old mutations went from goat-to-hero, providing just the designs that were needed to cope with the new environmental challenge. It was another example of the incredible serendipity that evolutionists call upon. Too good to be true? Not for evolutionists. The neutral theory became quite popular in the literature. The idea that mutations were not brimming with cool innovations but were mostly bad or at best neutral, for some, went from an anathema to orthodoxy. And the idea that those neutral mutations would later magically provide the needed innovations became another evolutionary just-so story, told with conviction as though it was a scientific finding. Another problem with the theory of neutral molecular evolution is that it made even more obvious the awkward question of where these genes came from in the first place. http://darwins-god.blogspot.com/2012/04/here-is-completely-different-way-of.html

as to drift

Thou Shalt Not Put Evolutionary Theory to a Test - Douglas Axe - July 18, 2012 Excerpt: "For example, McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time (i.e. the mutations cannot be 'neutral'). Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (greater than 100 million years). My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they're in the position of insisting that something is a scientific fact without having the faintest idea how it even could be." - Doug Axe PhD. http://www.evolutionnews.org/2012/07/thou_shalt_not062351.html Natural Selection Struggles to Fix Advantageous Traits in Populations - Casey Luskin - October 23, 2014 Excerpt: Michael Lynch, an evolutionary biologist at Indiana University,, writes that "random genetic drift can impose a strong barrier to the advancement of molecular refinements by adaptive processes."2 He notes that the effect of drift is "encouraging the fixation of mildly deleterious mutations and discouraging the promotion of beneficial mutations."3 Likewise, Eugene Koonin, a leading scientist at the National Institutes of Health, explains that genetic drift leads to "random fixation of neutral or even deleterious changes."4 http://www.evolutionnews.org/2014/10/natural_selecti_3090571.html

bornagain77

wd400 at 98, so you do not claim, as is held in the modern synthesis, that Body Plans are determined by DNA??? Really? I'm glad to hear that you do not since it is not true. But if mutations to DNA do not explain how a chimp-like creature can become a human, as they can't explain how it can happen, then why do you pretend as if you have proven how it can happen solely by reference to 15,000,000 mutations to DNA? Since mutations to DNA do NOT effect body plan morphogenesis, do I really need to point the fact out to you that there is a huge, gargantuan, gap in your explanation as to how we got here? A gargantuan gap that is very reminiscent of this cartoon??,,,

'Then a miracle occurs' - cartoon http://www.mcpsonline.org/images/f/f3/And_then_a_miracle_happens_cartoon.jpg

As to your unsubstantiated claim that most mutations are neutral, there are strong empirical and theoretical considerations for believing that there are no truly neutral nucleotide positions.

Unexpectedly small effects of mutations in bacteria bring new perspectives - November 2010 Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness. And this is the case regardless whether they lead to changes in the bacterial proteins or not.,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed. http://www.physorg.com/news/2010-11-unexpectedly-small-effects-mutations-bacteria.html "Moreover, there is strong theoretical reasons for believing there is no truly neutral nucleotide positions. By its very existence, a nucleotide position takes up space, affects spacing between other sites, and affects such things as regional nucleotide composition, DNA folding, and nucleosome building. If a nucleotide carries absolutely no (useful) information, it is, by definition, slightly deleterious, as it slows cell replication and wastes energy.,, Therefore, there is no way to change any given site without some biological effect, no matter how subtle." - John Sanford - Genetic Entropy and The Mystery of The Genome - pg. 21 - Inventor of the 'Gene Gun'

Moreover, neutral theory was not developed because of any empirical observation, but was developed because it was forced upon Darwinism by the mathematics. (i.e. neutral theory is actually the result of a theoretical failure of Darwinism!)

Haldane's Dilemma Excerpt: Haldane was the first to recognize there was a cost to selection which limited what it realistically could be expected to do. He did not fully realize that his thinking would create major problems for evolutionary theory. He calculated that in man it would take 6 million years to fix just 1,000 mutations (assuming 20 years per generation).,,, Man and chimp differ by at least 150 million nucleotides representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to been fixed by random drift - creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors - it surely would have killed us. Since Haldane's dilemma there have been a number of efforts to sweep the problem under the rug, but the problem is still exactly the same. ReMine (1993, 2005) has extensively reviewed the problem, and has analyzed it using an entirely different mathematical formulation - but has obtained identical results. John Sanford PhD. - "Genetic Entropy and The Mystery of the Genome" - pg. 159-160 Walter ReMine on Haldane's Dilemma - interview http://kgov.com/Walter-ReMine-on-Haldanes-Dilemma Kimura's Quandary Excerpt: Kimura realized that Haldane was correct,,, He developed his neutral theory in response to this overwhelming evolutionary problem. Paradoxically, his theory led him to believe that most mutations are unselectable, and therefore,,, most 'evolution' must be independent of selection! Because he was totally committed to the primary axiom (neo-Darwinism), Kimura apparently never considered his cost arguments could most rationally be used to argue against the Axiom's (neo-Darwinism's) very validity. John Sanford PhD. - "Genetic Entropy and The Mystery of the Genome" - pg. 161 - 162

A graph featuring 'Kimura's Distribution' being ‘properly used’ is shown in the following video:

Evolution Vs Genetic Entropy - Andy McIntosh - video https://vimeo.com/91162565

In fact neutral theory is why, against the overwhelming evidence now found for widespread functionality in the genome (i.e. ENCODE etc.. etc..), most neo-Darwinists still insist, against that overwhelming empirical evidence for widespread functionality, that most of the genome must be junk: At the 2:45 minute mark of the following video, the mathematical roots of the junk DNA argument, that is still used by many Darwinists, can be traced through Haldane, Kimura, and Ohno's work in the late 1950’s, 60’s through the early 70’s:

What Is The Genome? It's Not Junk! - Dr. Robert Carter - video - (Notes in video description) http://www.metacafe.com/w/8905583 Carter: Why Evolutionists Need Junk DNA - Robert W. Carter - 2009 Excerpt: Junk DNA is not just a label that was tacked on to some DNA that seemed to have no function, but it is something that is required by evolutionary theory. Mathematically, there is too much variation, too much DNA to mutate, and too few generations in which to get it all done. This was the essence of Haldane's work. Without junk DNA, evolutionary theory cannot currently explain how everything works mathematically. Think about it; in the evolutionary model there have only been 3-6 million years since humans and chimps diverged. With average human generation times of 20-30 years, this gives them only 100,000 to 300,000 generations to fix the millions of mutations that separate humans and chimps. This includes at least 35 million single letter differences, over 90 million base pairs of non-shared DNA, nearly 700 extra genes in humans (about 6% not shared with chimpanzees), and tens of thousands of chromosomal rearrangements. Also, the chimp genome is about 13% larger than that of humans, but mostly due to the heterochromatin that caps the chromosome telomeres. All this has to happen in a very short amount of evolutionary time. They don't have enough time, even after discounting the functionality of over 95% of the genome--but their position becomes grave if junk DNA turns out to be functional. Every new function found for junk DNA makes the evolutionists' case that much more difficult. Robert W. Carter - biologist http://creation.com/junk-dna-slow-death Kimura (1968) developed the idea of “Neutral Evolution”. If “Haldane’s Dilemma” is correct, the majority of DNA must be non-functional.

Here are more detailed refutations of 'neutral theory'

Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle - "Haldane's Ratchet" - Christopher L. Rupe and John C. Sanford - 2013 Excerpt: We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage. Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as "Haldane's Dilemma" is very real. Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon "Haldane's Ratchet". http://media.wix.com/ugd/a704d4_47bcf08eda0e4926a44a8ac9cbfa9c20.pdf Neo-Darwinism's Catch-22: Before Evolving New Features, Organisms Would Be Swamped by Genetic Junk - Casey Luskin - April 10, 2015 Excerpt: A new peer-reviewed paper in the journal Complexity presents a computational model of evolution which shows that evolving new biological structures may be deterred by an unavoidable catch-22 problem.,,, This is a bit complex -- let's go over it again. Darwinian evolution either (1) produces nothing new, or (2) it's destined to produce boatloads of deadly junk. In the case of (2), the reward for trying new things is high compared to the cost of building new structures. But in order for the ratio to be high enough for complexity to increase, the cost of building new things must be negligible. Novelties proliferate, but the fraction,, that's vestigial grows, and the organism is eventually swamped and overwhelmed by harmful vestigial features. However, if you try to avoid the problem of (2) by making the reward-to-cost ratio lower, as in (1), then nothing new ever evolves. The authors think real biological organisms are closer to position (1). Indeed, study in the field of systems biology increasingly finds that biological systems contain very little junk.,,, http://www.evolutionnews.org/2015/04/neo-darwinisms_095121.html

bornagain77

Just for the record, I would personally not be surprised if our DNA was once 100% identical with chimps, in the places that share sequence similarity. I fully accept the raw data and agree that where you can align bases between the genomes, they share 99% homology. But that does not mean our genomes are 99% the same - which is the picture it paints to the less discerning/knowledgable on genetics and science in general. I really would honestly not be surprised if a while back, chimps and humans as separate organisms existed where they both contained identical sequences in the alignable regions. Somewhere in Genesis 1-3, for example. Many IDists and even YECs have absolutely no problem with high homology even with chimps. It is hardly unexpected. Dr JDD

JDD, I discussed what the different estiamtes from the literature mean in 17 and 24. The 99% is not a myth, it’s one accurate description of how similar our genes are. The 2.4Gb was the size of the chimp reference genome at that time (representing the work in progress nature of the genome, and the fact the chimp sequence is much worse than either the human or the gorilla). The human and chimps genomes are both about 3.5 pg (I think the best estimate of chimp is 3.45.

WD400, I'm confused. Did they in 2005 believe that the chimp genome was in fact 2.55 Gbp? Were they really nearly ~0.9-0.95Gbp out from what we think now? You state:

The 2.4Gb was the size of the chimp reference genome at that time

And in the publication they state:

The draft genome assembly—generated from ~3.6-fold sequence redundancy of the autosomes and ~1.8-fold redundancy of both sex chromosomes—covers ~94% of the chimpanzee genome with >98% of the sequence in high-quality bases.

So they claim to cover 94% of the chimp genome. They then state:

We set out to study the mutational events that have shaped the human and chimpanzee genomes since their last common ancestor. We explored changes at the level of single nucleotides, small insertions and deletions, interspersed repeats and chromosomal rearrangements. The analysis is nearly definitive for the smallest changes, but is more limited for larger changes, particularly lineage-specific segmental duplications, owing to the draft nature of the genome sequence. Nucleotide divergence Best reciprocal nucleotide-level alignments of the chimpanzee and human genomes cover ~2.4?gigabases (Gb) of high-quality sequence, including 89?Mb from chromosome X and 7.5?Mb from chromosome Y.

So again, I come back to the point - it seems here they are: 1) Stating their OWN results and alignment with the human genome as 2.4Gb of sequence aligned 2) Stating that they cover ~94% of the chimp genome Now if the genome of the chimp is in fact 3.45Gb, then this does not quite add up. Either they should be shot for incredibly bad wording, or you are wrong with what you say, or back in 2005 they significantly underestimated the size of the chimp genome, by 25%. Which is it? Because 3.45 x 0.94 (x 0.98 for high quality) does not equal 2.4. It equals 3.17. So why can they only align 2.4Gb? I don't understand this. Maybe they underestimated the size of the whole chimp genome but that is not clear to me. Secondly, you state:

The 99% is not a myth, it’s one accurate description of how similar our genes are.

Do you really mean that sentence in the implication of its words? Do you understand that people are generally not contesting that notion? I know you have said slightly different elsewhere in the thread but I would have thought you would be more careful if so - not many are contesting that we are 99% identical to chimps in our genes. For we all know the definition of "gene". And barely anyone here will argue with you over our similarity of genes, but rather the genome. Further, the whole point is sloppy science. Many people (I'll exclude you from this as I have read numerous, numerous atheistic evolutionary biologists say this) will state anywhere from 90% same DNA to chimps to 96%, to 98%. These are people who do NOT support ID. Many do not adhere to the 99% line. And yet, even if we were 99% chimps and humans cary dramatically. As said, that is what the contentious point is - that different cannot be simply due to 1% of the genome. If it is, we really do not understand the genome well at all, if it is not, the Darwinian paradigm falls quite flat. So to sloppily say we are "99% the same" as so many pop-science articles do is quite frankly, silly, and shows a brainwash of the media towards the Darwinian worldview as being gospel. Dr JDD

The only assumption in that calculation is the one I stated -- that new mutaitions are selectively neutral. Positive selection of the sort discussed in your links might make more mutations fix, but the neutral rate is equal to the per-individual mutation rate. wd400

wd400 claims:

Well, 30 million differences = 15 million changes in each lineages. Absent selection changes fix at a rate equal to the per-individual mutation rate. Taking a 20 year generation time you have 6 Million years / 20 years/gen = 300 000 generations 15 million mutations / 300 000 generations = 50 mutations/generations Which is pretty much what he observe! Care to withdraw?

What wd400 does not inform people of are the hidden assumptions built into his 'back of the envelope' calculation. One hidden assumption is the claim that changes to DNA can effect body plan morphogenesis, which is a claim he simply has no evidence for:

Response to John Wise - October 2010 Excerpt: A technique called "saturation mutagenesis"1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans--because none of the observed developmental mutations benefit the organism. http://www.evolutionnews.org/2010/10/response_to_john_wise038811.html

Another hidden assumption in wd400's 'back of the envelope' calculation is that most all of the 15,000,000 mutations will be 'fixed' fairly easily. He simply has no evidence for that assumption:

More from Ann Gauger on why humans didn’t happen the way Darwin said - July 9, 2012 Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population. You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/ Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies http://eebweb.arizona.edu/nachman/Suggested%20Papers/Lab%20papers%20fall%202010/Burke_et_al_2010.pdf

In fact, the types of mutations that will most easily fix are NOT the types of mutations that wd400 needs:

“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Getting There First: An Evolutionary Rate Advantage for Adaptive Loss-of-Function Mutations Michael J. Behe - 2013 http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0020 Biological Information - Loss-of-Function Mutations by Paul Giem 2015 - video playlist (Behe - Loss of function mutations are far more likely to fix in a population than gain of function mutations) https://www.youtube.com/watch?v=hzD3hhvepK8&index=20&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ Study demonstrates evolutionary ‘fitness’ not the most important determinant of success – February 7, 2014 – with illustration Excerpt: An illustration of the possible mutations available to an RNA molecule. The blue lines represent mutations that will not change its function (phenotype), the grey are mutations to an alternative phenotype with slightly higher fitness and the red are the ‘fittest’ mutations. As there are so few possible mutations resulting in the fittest phenotype in red, the odds of this mutation are a mere 0.15%. The odds for the slightly fitter mutation in grey are 6.7% and so this is far more likely to fix, and thus to be found and survive, even though it is much less fit than the red phenotype.,,, By modelling populations over long timescales, the study showed that the ‘fitness’ of their traits was not the most important determinant of success. Instead, the most genetically available mutations dominated the changes in traits. The researchers found that the ‘fittest’ simply did not have time to be found, or to fix in the population over evolutionary timescales. http://phys.org/news/2014-02-evolutionary-important-success.html This following headline sums the preceding finding up very nicely: Fittest Can’t Survive If They Never Arrive – February 7, 2014 http://crev.info/2014/02/fittest-cant-survive-if-they-never-arrive/

There is much more that is fallacious in wd400's thinking, but I will leave the refutation of his claim at this stage for the moment and give him a chance to respond to Behe, Gauger and Axe. bornagain77

wd400 is determined to beat a dead horse so, once again, here is Tomkins's paper where the unbiased reader can judge for themselves who is being forthright and who is being biased towards the evidence.

Comprehensive Analysis of Chimpanzee and Human Chromosomes Reveals Average DNA Similarity of 70% by Jeffrey P. Tomkins on February 20, 2013 Abstract Since the original 2005 report for the chimpanzee (chimp) genome assembly (5X rough draft), an additional one-fold redundant coverage has been added. Using the new 6X chimpanzee assembly, a sequential comparison to the human genome was performed on an individual chromosome basis. The chimpanzee chromosomes, were sliced into new individual query files of varying string lengths and then queried against their human chromosome homolog using the BLASTN algorithm. Using this approach, queries could be optimized for each chromosome irrespective of gene/feature linear order. Non-DNA letters (gap filling ‘N’s) were stripped from the query data and excluded from the analyses. The definition of similarity for each chromosome was the amount (percent) of optimally aligned chimp DNA. This definition was considered to be conservative because it did not include the amount of human DNA absent in chimp nor did it include chimp DNA that was not aligned to the human genome assembly (unanchored sequence contigs). For the chimp autosomes, the amount of optimally aligned DNA sequence provided similarities between 66 and 76%, depending on the chromosome. In general, the smaller and more gene-dense the chromosomes, the higher the DNA similarity—although there were several notable exceptions defying this trend. Only 69% of the chimpanzee X chromosome was similar to human and only 43% of the Y chromosome. Genome-wide, only 70% of the chimpanzee DNA was similar to human under the most optimal sequence-slice conditions. While, chimpanzees and humans share many localized protein-coding regions of high similarity, the overall extreme discontinuity between the two genomes defies evolutionary timescales and dogmatic presuppositions about a common ancestor. https://answersingenesis.org/answers/research-journal/v6/comprehensive-analysis-of-chimpanzee-and-human-chromosomes/

Please note that ORFans were excluded from the above analysis: (i.e. This definition was considered to be conservative because it did not include the amount of human DNA absent in chimp nor did it include chimp DNA that was not aligned to the human genome assembly (unanchored sequence contigs).) And here is another recent paper by Tomkins which underscores the point made in the previous paper:

Comparison of the Transcribed Intergenic Regions of the Human Genome to Chimpanzee - Jeffrey P. Tomkins - 2014 Abstract: The human genome is pervasively transcribed and produces a wide array of long noncoding RNAs that have been implicated in gene regulation, chromatin modification, nuclear organization, and scaffolding for functionally active protein complexes. Of particular interest in human origins is the long and very long intergenic noncoding RNAs transcribed from genomic regions outside protein coding genes. These are known as lincRNA and vlincRNA, respectively. Linc­RNA regions of the genome are more taxonomically restricted than protein coding segments and make logical candidates for research in genomic discontinuity. This report describes the comparative use of three different human lincRNA datasets and one vlincRNA dataset to the chimpanzee genome using the BLASTN algorithm. Short human lincRNA genomic regions (less than 600 bases) were about 75–79% similar to chimpanzee, while the larger lincRNA regions (greater than 600 bases) were about 71 to 74% similar. The human vlincRNA genomic regions were only 67% similar to chimpanzee. In contrast, all known human protein coding exons 300 to 599 bases in length, are 86% similar to chimpanzee. https://www.creationresearch.org/images/CRSQ-PDFs/Public-Articles/CRSQ-50-04-Tomkins.pdf

And here is a repost of the video interview of Tomkins where a person can see for themselves the integrity and professionalism with which Tomkins conducts himself.

The Myth of 98% Genetic Similarity between Humans and Chimps – Jeffrey Tomkins PhD. – video https://vimeo.com/95287522

bornagain77

unwilling participant- Dr Denton puts that to rest in his article in "Uncommon Dissent":

To understand the challenge to the “superwatch” model by the erosion of the gene-centric view of nature, it is necessary to recall August Weismann’s seminal insight more than a century ago regarding the need for genetic determinants to specify organic form. As Weismann saw so clearly, in order to account for the unerring transmission through time with precise reduplication, for each generation of “complex contingent assemblages of matter” (superwatches), it is necessary to propose the existence of stable abstract genetic blueprints or programs in the genes- he called them “determinants”- sequestered safely in the germ plasm, away from the ever varying and destabilizing influences of the extra-genetic environment. Such carefully isolated determinants would theoretically be capable of reliably transmitting contingent order through time and specifying it reliably each generation. Thus, the modern “gene-centric” view of life was born, and with it the heroic twentieth century effort to identify Weismann’s determinants, supposed to be capable of reliably specifying in precise detail all the contingent order of the phenotype. Weismann was correct in this: the contingent view of form and indeed the entire mechanistic conception of life- the superwatch model- is critically dependent on showing that all or at least the vast majority of organic form is specified in precise detail in the genes. Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype. The emerging picture made it increasingly difficult to see genes as Weismann’s “unambiguous bearers of information” or view them as the sole source of the durability and stability of organic form. It is true that genes influence every aspect of development, but influencing something is not the same as determining it. Only a small fraction of all known genes, such as the developmental fate switching genes, can be imputed to have any sort of directing or controlling influence on form generation. From being “isolated directors” of a one-way game of life, genes are now considered to be interactive players in a dynamic two-way dance of almost unfathomable complexity, as described by Keller in The Century of The Gene.

It's not the genes. It ain't the genome. It ain't the same ole genes used differently. And that is the main reason why evolutionism is a failure. In his book (English title) “Why is a Fly not a Horse?”, the prominent Italian geneticist Giuseppe Sermonti, tells us the following : Chapter VI “Why is a Fly not a horse?” (same as the book’s title)

”The scientist enjoys a privilege denied the theologian. To any question, even one central to his theories, he may reply “I’m sorry but I do not know.” This is the only honest answer to the question posed by the title of this chapter. We are fully aware of what makes a flower red rather than white, what it is that prevents a dwarf from growing taller, or what goes wrong in a paraplegic or a thalassemic. But the mystery of species eludes us, and we have made no progress beyond what we already have long known, namely, that a kitty is born because its mother was a she-cat that mated with a tom, and that a fly emerges as a fly larva from a fly egg.”

Joe

I think that genes do determine “what” will develop. The environment can only have an impact on how these genes are expressed

They do not know where the instructions are for construction of a complex organism. They are somewhere in the egg but they are not sure where. Probably in cellular wall. jerry

Joe: "There aren’t any such genes. What makes us human is not found in the genes nor how they are regulated. Genes influence development but they do not determine what will develop." I don't see how you figure this. If you implant a tiger fetus in a lion, the outcome is a tiger. I think that genes do determine "what" will develop. The environment can only have an impact on how these genes are expressed. unwilling participant

What shall we say about the genes which make us human?

There aren't any such genes. What makes us human is not found in the genes nor how they are regulated. Genes influence development but they do not determine what will develop. Joe

Found reference: www.asa3.org/ASA/meetings/belmont2013/papers/ASA2013Wilcox.pdf One of the things it says is that the regulatory nature in the human genome is extremely more complex than the next species. Here is a quote:

What shall we say about the genes which make us human? We and chimps share 96% to 99% of our protein coding sequences. Why are we different? Not the 1.5% of our genome that codes for proteins but the 98.5% that controls their production. Literally, no other primate lineage has evolved as fast as our lineage has during the last 1.5 million years, and it’s all due to unique changes in our control genome. At least 80% probably more of our “non-coding” genome is also transcribed, starting from multiple start points, transcribed in both directions, with overlapping reading frames of many sizes and a whole spectrum of alterations, producing a whole zoo of ‘new’ types of RNA control elements – piRNA,siRNA, miRNA,sdRNA, xiRNA, moRNA, snoRNA, MYS-RNA, crasiRNA, TEL-sRNA, PARs, and lncRNA. Most of these unique RNA transcripts – and there are thousands, if not millions of them – are uniquely active in developing human neural tissue – uniquely active compared to their activity in chimpanzees, much less other primates or mammals. It is the new epigenetic world

jerry

What a lot of noise. Q,

I see. So is this the data that wd400 has been referencing that shows that the parts of human DNA that matches chimpanzee DNA matches up extremely closely?

Nope, i've linked to the raw data several times. Anyone that wants to check it out can.

* What percent of closely matching dolphin DNA matches that of human DNA? * And what percent of closely matching dolphin DNA matches chimpanzee DNA? * Is this technique broadly used to determine evolutionary relationships?

About 75%. About 75%. Not really, but that both chimps and humans (and organs and gorillas and monkeys...) have about the same similatity to a all the ungulates (dolphins included) is certainly easier to explain under common descent than other proposals.

Even if there was a 99% similarity between chimes and humans which there aren’t it still means a staggering 30 000 00 base pair difference. Consider that our last common ancestor lived a about 6 000 000 years ago Darwinism still can’t explain the amount of changes in such a short geological blink of time. WD400 the floor is yours. Enlighten us.

Well, 30 million differences = 15 million changes in each lineages. Absent selection changes fix at a rate equal to the per-individual mutation rate. Taking a 20 year generation time you have 6 Million years / 20 years/gen = 300 000 generations 15 million mutations / 300 000 generations = 50 mutations/generations Which is pretty much what he observe! Care to withdraw? JDD, I discussed what the different estiamtes from the literature mean in 17 and 24. The 99% is not a myth, it's one accurate description of how similar our genes are. The 2.4Gb was the size of the chimp reference genome at that time (representing the work in progress nature of the genome, and the fact the chimp sequence is much worse than either the human or the gorilla). The human and chimps genomes are both about 3.5 pg (I think the best estimate of chimp is 3.45. wd400

i am writing from an iPad and away from home so am limited in resources. I believe the really big differences between chimps and humans are in the control mechanisms not in the protein coding sequences. Especially the control of neural areas of the brain. jerry

Mung:

wd400: What interests me is how anti-scientific movements propagate. Then why are you wasting your time at this site? Go find a movement that’s anti-science.

The astonishing thing is that Darwinism is the most anti-scientific movement in the history of humanity. Mapou

wd400: What interests me is how anti-scientific movements propagate. Then why are you wasting your time at this site? Go find a movement that's anti-science. Mung

The post by Timaeus @76 is well worth reading. Mung

Timaeus:

Indeed, the whole AGW propaganda machine has been an object lesson in how to spread extremely shaky science (mathematical models based on many questionable factual assumptions and at most about a 20% understanding of the complex causes of global climate change) and get it treated by the intelligentsia of the West as Gospel truth.

Meanwhile the Zombie threat is very real: The Equation That Can Help Predict Zombie Migration Patterns Mung

KevNick

Since Darwinists believe that the evolution is all about genes, why can’t they tweak the chimpanzee genome in the lab and make it at least to wipe after they take a dump?

I don't think that this is what evolutionists believe. It is my understanding that they believe it is about the affect of the environment on the expression of genes. unwilling participant