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Thursday, January 31, 2013

Theme: Mutation

This is a collection of Sandwalk posts on mutation starting in 2007. The latest ones are at the bottom of the list.

March 27, 2007
Silent Mutations and Neutral Theory
Neutral Theory and random genetic drift explains variation and it also explains molecular evolution and the (approximate) molecular clock. There are no other explanations that make sense and nobody has offered a competing explanation since Motoo Kimura (1968) or Jack King and Thomas Jukes (1969) published their papers almost fifty years ago. (Aside from occasional nitpicks, of course. There are always scientists who like to show that some mutations that were thought to be neutral are actually beneficial or deleterious. None of them have mounted a serious claim that most variation or most of molecular evolution can be explained by natural selection.)

April 19, 2007
Haldane's Dilemma
This is very interesting. Dembski has teamed up with Walter ReMine, demonstrating once again that the old addage "opposites attract" does not apply to kooks.

ReMine has an article on Uncommon Descent where he pushes his usual whine about evil scientists and how their world-wide conspiracy has kept him from revealing the fatal flaw in evolution [Evolutionist withholds evidence on Haldane’s Dilemma]. I can see how similar this is to Intelligent Design Creationism.

Calculating the rate of evolution in terms of nucleotide substitutions seems to give a value so high that many of the mutations must be neutral ones.

Motoo Kimura (1968)
July 5, 2007
Mutation Rates
The most common source of mutation is due to mistakes made during DNA replication when an incorrect nucleotide is incorporated into newly synthesized DNA. The mutation rate due to errors made by the DNA polymerase III replisome is one error for every one hundred million bases (nucleotides) that are incorporated into DNA. This is an error rate of 1/100,000,000, commonly written as 10-8 in exponential notation. Technically, these aren't mutations; they count as DNA damage until the problem with mismatched bases in the double-stranded DNA has been resolved. The DNA repair mechanism fixes 99% of this damage but 1% escapes repair and becomes a mutation. The error rate of repair is 10-2 so the overall error rate during DNA replication is 10-10 nucleotides per replication (10-8 × 10-2) (Tago et al., 2005).

December 3, 2007
Seymour Benzer (1921 - 2007)
Seymour Benzer died last Friday. In the 1950's and 1960's Benzer was a prominent member of the 'phage group founded by Max Delbrück and Salvador Luria [The Nobel Prize in Physiology or Medicine 1969.].

Benzer was best known for his detailed mapping of the rII locus in bacteriophage. Benzer was able to resolve mutants that were likely to be only a single nucleotide apart. His work on mapping deletions led directly to the conclusion that the genetic codon should consist of three nucleotides. In honor of Seymour Benzer, John Dennehy has selected his 1955 paper as this week's citation classic [Benzer, S. (1955)].

December 11, 2007
Accelerated Human Evolution
We frequently hear claims that humans have stopped evolving. Most of these claims have to do with medical advances that are now allowing people to survive who might have died in earlier times. The idea is that natural selection is no longer working so we have stopped evolving.

This is a flawed argument [Have Humans Stopped Evolving?]. Assuming that medical advances are having a significant impact on the world's population, it follows that the impact is to speed up evolution and not slow it down!

March 14, 2008
Evolution and Variation in Folded Proteins
Data like this reveals that the amino acid residues in the active site are usually conserved. Residues in the hydrophobic core are moderately conserved. And residues on the surface are hardly conserved at all.

The point is that there are literally billions of different proteins that have the same shape as globins and still function as carriers of oxygen. This is an important point. Opponents of evolution often take a single globin from a single species and calculate the probability that such a structure will form. They assume that only one out of twenty amino acids can be found at each position and the resulting probability (e.g., 20020) is enormous. Thus, they conclude, such a protein could never form by chance. They don't seem to appreciate the fact that we already know of billions of different proteins that can function as globins.

May 14, 2008
Nobel Laureates: George Beadle and Edward Tatum
George Wells Beadle (1903 - 1989) and Edward Lawrie Tatum (1909 - 1975) received the Nobel Prize in Physiology or Medicine for their work on the relationship between genes and enzymes—the "one-gene-one-enzyme" concept. They showed that single mutations usually affected production of a single enzyme in a pathway. This lead to the idea that genes encode proteins (enzymes). The concept of one-gene-one-enzyme was not meant to exclude the possibility that genes could encode RNAs or something else, in spite of the fact that this interpretation has become widely believed. The point of Beadle and Tatum's work was to show that there was a one-to-one correspondence between a gene and a protein.

July 12, 2008
The Fluctuation Test
John Dennehy of The Evilutionary Biologist continues his almost perfect1 record of picking important papers for his Citation Classic.

This week's paper is the classic 1943 paper by Luria and Delbrück on the fluctuation test [The Fluctuation test]. This was the paper that proved that mutations arise randomly with respect to their phenotype. As John says, it is one of the most important experiments in biology.

October 7, 2008
Steve Jones Says Human Evolution Is Over
There's so much wrong with this article by Steve Jones that I don't know where to begin. So I'll leave it up to Sandwalk readers to comment. Steve Jones is a Professor of genetics at University College, London (UK) and the author of Darwin's Ghost.

From Times Online via

October 16, 2008
Nobel Laureates: Christiane Nüsslein-Volhard and Eric Wieschaus

Christiane Nüsslein-Volhard (1942 - ) and Eric F. Wieschaus (1947 - ) received the Nobel Prize in Physiology or Medicine for their contribution to understanding the genetics of development in the fruit fly, Drosophila melanogaster.

Their main contribution was to identify a number of genes that controlled the development of the embryo. The approach was to create mutations at random then screen large numbers of flies for recessive lethals affecting various stages of early embryogenesis. The initial large scale experiment was carried out at the EMBL Labs in Heidleberg, Germany. They established 27,000 lines containing mutated chromosomes and characterized 139 mutations affecting embryogenesis. Of these, 15 were described in the classic 1980 Nature paper. (See Silver Screen, a tribute to the paper on it's 25th anniversary.)

October 16,2008
Balancer Chromosomes
The chromosomes shown here are the large polytene chromosomes of the salivary glands. They are made up of 1000-2000 aligned stands of DNA that form when successive rounds of DNA replication are not followed by separation of cell division. Flies that are heterozygous for a wild type chromosome and one with a large deletion inversion, will form the loop structure shown in the diagram.

In normal cells, you won't see this structure as the chromosomes align during mitosis and meiosis, but it still exists. What the structure tells us is that the presence of an inversion, or any other type of chromosomal rearrangement for that matter, doesn't have much effect on chromosomal alignment and segregation during cell division.

October 21, 2008
Hermann Muller Invented the Balancer Chromosome
Since writing about Balancer Chromosomes, I've gotten several email messages pointing out things I missed. Thanks to everyone who responded. It's what makes this blog worthwhile.

Quite a few readers pointed out that balancer chromosomes were invented a very long time ago by Hermann Muller. Muller won the Nobel Prize in 1946 for discovering mutagenesis by X-rays.

March 6, 2009
Are Humans Still Evolving?
This is a follow-up to my earlier posting about the latest issue of Discover magazine [Ascent of Darwinism]. I want to discuss another article in that issue: "Are We Still Evolving" by Kathleen McAuliffe. The title of the web version is: They Don't Make Homo Sapiens Like They Used To.

In a minute we'll look at the quality of science journalism in this article, but first a little background.

March 9, 2009
Did biologists really think that human evolution stopped?
John Hawks has responded to my posting on the Discover article. In that posting [Are Humans Still Evolving?] I criticized Hawks and his colleagues for claiming that the consensus view among scientists is that human evolution is over.

Recall that the opening sentence of the article is ... "For decades the consensus view—among the public as well as the world’s preeminent biologists—has been that human evolution is over."

March 12, 2009
Examples of Accelerated Human Evolution
Gregory Cochran and Henry Harpending claim that human evolution has accelerated in the last 10,000 years. In one sense this has to be correct since the number of humans is increasing exponentially and that means far more mutations are occurring every generation. Many of those new mutations are contributing to a significant increase in variation.

But that's not what they mean. They claim that adaptations have increased. When they talk about accelerated human evolution they are mostly talking about an increase in natural selection.

June 30, 2009
Genes, Phylogeny, and Orangutans
Jeffrey H. Schwartz is well known to veterans because we discussed his book (Sudden Origins: Fossils, Genes, and the Emergence of Species) back in 1999. Schwartz tried to make the case for a "groundbreaking and radical new theory of evolution." This "theory" was based on the idea that new species spring into existence very quickly when a mutation in a homeobox (HOZ) gene arises in a population. It's a "theory" of saltation but it's based on such a flawed understanding of genetics that you really have to read to book to see just how bad it is. Sudden Origins is a leading candidate for the worst science book ever published.

September 1, 2009
Human Y Chromosome Mutation Rates
One thing men are really good at is making mistakes—just ask any woman. When it comes to mutations we are ten times better than women at ensuring the evolution of the species.

Knowing the actual rate of mutation in humans—or any other species—is important for many reasons. For one thing, it tells us about the maximum possible rate of evolution. For another, it gives us an important clue about the differences between beneficial, detrimental, and neutral alleles.

September 15, 2009
Chromosomes, Drift, and Demes
One of the characteristics of evolution is change in chromosome number and organization. These large-scale changes are often associated with speciation events although it would be a mistake to assume that there's a causal relationship.

One particular chromosomal rearrangement has been getting a lot of press recently because it has been featured on blogs and in some recent trade books on evolution.

Humans (H) have only 23 pairs of chromosomes while most other apes, such as the chimpanzee (C), have 24 pairs.

September 29, 2009
You Can't Go Home Again
Glucocorticoid receptor specifically binds cortisol but the ancient protein binds other steroids as well as cortisol. This is pretty much what you might expect. Various gene duplication events lead to a family of proteins and each family member evolved to recognize a single ligand. The fact that you can reconstruct the presumed ancestral protein and show that it bound to multiple ligands is pretty amazing. The work comes out of Joseph Thornton's lab (Ortlund et al. 2007).

Altogether there were about 60 amino acid substitutions along the lineage leading from the ancestral broad-specificity receptor to the cortisol-specific receptor but only two of these turned out to be ones that shifted the specificity. Most of the rest probably had little effect of the function or specificity of the protein. This is the expected result. Most amino acid substitutions during evolution are neutral.

October 16, 2009
Joe Thornton vs Michael Behe
A few weeks ago I blogged about an important series of papers on the evolution of the glucocorticoid receptor gene [see You Can't Go Home Again]. This is work from the Thornton lab and it shows the effect of accumulating neutral mutations over millions of years. I like the papers because it demonstrates clearly where Michael Behe goes wrong in his latest book The Edge of Evolution.

Carl Zimmer liked the papers as well and he wrote about them in a great big blog called The New York Times [see Can Evolution Run in Reverse? A Study Says It’s a One-Way Street]. I hate it when he does that. It makes me look bad.

October 22, 2009
Evolution in Action and Michael Behe's Reaction
Much of the paper is about adaptive vs. non-adaptive mutations. At 40,000 generations there were 627 SNP and 26 DIP mutations. The increase was due, in part, to an increase in mutation rate because of a mutation in the mutT gene. One might expect that the initial adaptation would result in selection for beneficial alleles and that neutral alleles would accumulate by random genetic drift in subsequent generations (i.e. from 20K generations to 40K generations). This is probably what happened from 20K generations to 40K generations.

November 17, 2009
Genetic Load, Neutral Theory, and Junk DNA
A species cannot afford to accumulate deleterious mutations in the genomes of its individuals. Eventually the number of "bad" mutations will reach a level where most genes have multiple "bad" alleles and it becomes impossible to produce offspring.

This phenomenon is referred to as genetic load. It means that species can only survive if the genetic load is below some minimum value. A good rule of thumb is that there can't be more than 0.1 deleterious mutations per individual per generation but in actual populations this value can be a bit higher.

December 15, 2009
Does Excess Genomic DNA Protect Against Mutation?
One of the adaptive explanations for this excess DNA is that it protects the functional DNA from mutations. Ryan Gregory thinks this is a serious scientific hypothesis even though he's skeptical. He has a wonderful post that reviews the history of the idea and how the hypothesis should be tested [Does junk DNA protect against mutation?].

The bottom line is that this hypothesis is not taken very seriously by the scientific community for some very good reasons.

The main reason, in my opinion, that the process of science has gone so badly off track in evolutionary biology is the success of the Modern Synthesis.

Arlin Stoltzfus
March 19, 2010
Introduction to "The Curious Disconnect"
Arlin Stoltzfus says,
This way of thinking suggested that mutational-developmental bias in the introduction of variation was a general cause of evolutionary bias or direction. That contradicted two things I knew about evolutionary thinking. First, I knew that the notion of "internal" variational causes of direction, called "orthogenesis", had been rejected as a heresy. Second, I knew that, among contemporary researchers, mutation bias was not seen as a general bias on the course of evolution, but as a special aspect of neutral evolution, incompatible with selection.
March 19, 2010
Direct Measurement of Human Mutation Rate
A recent paper in Science attempted a direct measurement of the mutation rate by comparing the complete genome sequences of two offspring and their parents. They estimate that each offspring had 70 new mutations (instead of the predicted 130) for a mutation rate of 1.1 × 10-8 per haploid genome per generation (Roach et al. 2010).

The mutationism myth tells the story of how, just over a century ago, the scientific community responded to the discovery of Mendelian genetics by discarding Darwinism, and how Darwinism subsequently was restored.March 30, 2010
The "Mutationism" Myth I. The Monk's Lost Code and the Great Confusion
Arlin Stoltzfus says,
Our journey to explore The Curious Disconnect-- the gap between how we think about evolution and how we might think if we were freed from historical baggage-- begins with the Mutationism Myth. In this, the first of four parts, we are not going to confront any tough scientific or conceptual issues. Instead, we are just going to review an odd story about our intellectual history.
May 4, 2010
The Mutationism Myth, II. Revolution
Arlin Stoltfus says,
Our journey to map out the Curious Disconnect— the gap between how we think about evolution and how we might think if we were freed from historical baggage— began with The Mutationism Myth, part 1. Then, in Theory vs Theory, we took a brief detour to distinguish theory1 (grand conjecture) from theory2 (body of abstract principles). Today we are back to the Mutationism Myth and our goal is to probe its claim that the scientific community rejected Darwin's ideas on erroneous grounds.
May 20, 2010
The Mutationism Myth: III Foundations of Evolutionary Genetics
Arlin Stoltfus says,
Today in the Curious Disconnect we continue with our series on the Mutationism Myth. In this oft-told story (see part 1), the discovery of genetics in 1900 leads to rejection of Darwin's theory and the rise of "mutationism", a laughable1 theory that imagines evolution by mutation alone, without selection. "Mutationism" prevails for a generation, until Fisher, Haldane and Wright show that genetics is the missing key to Darwinism. In the conclusion to the story, the world is set right again when the "Modern Synthesis", combining selection with Mendelian genetics, shoulders aside the mutationist heresy, which ends up in the dustbin of history with the other "doomed rivals" of Darwin's great theory.
May 30, 2010
Calibrating the Molecular Clock
John Hawks is discussing the evolution of hominids on his blog and, in particular, whether Ardipithecus (Ardi) is a hominid [Ardipithecus challenge explication: the molecular clock].

This is a complex issue. One of the problems is that Ardi is supposed to have lived 5.5 million years ago, according to John Hawks, but all estimates of the human-chimp divergence say it occurred between 3 and 5 million years ago. If that's true then Ardi is not in either the chimp or human lineages.

June 3, 2010
The Mutationism Myth, IV: Mendelian Heterodoxies
Arlin Stoltfus says,
The reader who has been following our story so far may be baffled. As we found out in part 3, the Mendelians understood how to conceptualize a population as a dynamic system of allele and genotype frequencies (the Bateson-Saunders equilibrium), how to see evolutionary change as a probabilistic 2-step process of the introduction and acceptance-or-rejection of mutations, and how to think about selection-driven changes in a quantitative trait.

Why don't the Mendelians get credit for laying the foundations of the 20th-century consensus?

June 22, 2010
The Mutationism Myth, V: The response to Mendelian heterodoxies
This is the seventh in a series of postings by guest blogger, Arlin Stoltzfus.

Deconstructing The Mutationism Myth erodes the conventional wisdom about the early Mendelians, and also exposes the incompatibility with genetics that led the Mendelians to reject Darwin's theory. As we will see today on the Curious Disconnect (credits), unraveling the Mutationism Myth also puts the Modern Synthesis in a new light.

August 31, 2010
The Mutationism Myth, VI: Back to the Future
This is Arlin's last contribution. The entire series has been an excellent introduction to the history of evolutionary theory and the concept of mutationism. There are many ways in which the so-called "Modern" Synthesis has to be revised and extended. One of them is to reinstate the concept of mutationism which was purged from evolutionary theory in the 1940s. If you want to understand why this is important then these articles are the place to start.

September 5, 2010
Mutation and Intelligent Design Creationism
One of the long-standing criticisms of Intelligent Design Creationists is their continuing effort to confuse the general public about modern evolutionary theory. Here's the latest effort by "johnnyb," just posted on Uncommon Descent [Responding to Merlin Part I – How Merlin’s Paper Validates Several Claims of the ID Movement].

The article discusses a recent paper by Francesca Merlin1 from the Department of Philosophy, University of Montréal, Québec, Canada [Evolutionary Chance Mutation: A Defense Of the Modern Synthesis’ Consensus View]. Note the title. She is defending the "Modern Synthesis' Consensus View."

September 8, 2010
Mutations and Complex Adaptations
Michael Lynch is one of those rare scientists who not only think outside the box but successfully stimulate others to do so. I read all of his papers and I'm always very impressed, even though I don't always agree with everything he says.

I recently attended the 18th Annual Meeting of the Society for Molecular Biology and Evolution in Lyons, France, where I met Michael Lynch for the first time. He gave a talk on Evolution of Mutation Rates, a topic many of us treat with a large degree of skepticism—until we're confronted by Michael Lynch. He makes a convincing case for variable rates of mutation in different species and he challenged us (me) to defend the idea that there was a linkage between DNA replication rates and mutation rates. That's a linkage I've always assumed would constrain mutation rates to a narrow range. Now I'm not so sure.

October 5, 2010
The Edge of Evolution
Behe's version of the history of life requires a God who intervenes quite frequently to create specific mutations that are almost impossible to account for by random mutation. Behe makes a good case for the problems with random mutation. In fact, his arguments are similar to those put forth by the mutationist camp—a group that I'm in sympathy with. Most biologists would not be able to refute Behe's arguments because they would agree with some of his false premises.

Behe's "Two Binding Sites Rule" is a good example. He argues that in order for two proteins to interact, evolution needs to create a small patch on the surface of each protein where five or six amino acid side chains become compatible with binding. Some of these changes could be neutral so they could arise independently but the analysis of hundreds of known binding sites shows that many of the mutations would be detrimental if they occurred by themselves—a single charged amino acid residue on the surface, for example.

November 4, 2010
Human Mutation Rates
The other study, by Roach et al. (2010), compared the genome sequences of two offspring and their parents. By adding up all the differences in the offspring they arrived at an estimate of 70 mutations in the offspring instead of the expected 130 [Direct Measurement of Human Mutation Rate]. This is half the expected value but the study is fraught with potential artifacts and it's best not to make a big deal of this discrepancy.

John Hawks was worried about this last March [A low human mutation rate may throw everything out of whack ] and he's still worried about it today [What is the human mutation rate?].

November 13, 2011
Jonathan Wells Talks About Genetic Load
The genetic load argument dates from the late 1960s when several experts in molecular evolution realized that humans could not survive if most of their genome was susceptible to mutation. They calculated that only small percentage could actually be functional and the majority had to be impervious to nucleotide substitutions and insertion/deletions.

The argument is based on the rate of mutation, which is largely due to DNA replication errors. The biochemistry is very well understood [Mutation Rates]. All recent data on genome sequencing confirms the mutation rate; the only scientific controversy is whether it could be as much as 2× higher than the biochemstry suggests. That dispute doesn't have any significant affect on the genetic load argument.

January 20, 2012
Understanding Mutation Rates and Evolution
But let's not quibble about the actual example that Behe uses. The principle is sound; namely, that there almost certainly are examples where a double mutation will be beneficial but each individual mutation is detrimental. The probability that the two mutations will arise simultaneously in the same individual is 10-20 as Behe says. If that's what has to happen then this really is beyond the edge of evolution ... or is it?

No, it's not. It's not true that deleterious mutations are quickly eliminated from a population. According the modern Nearly Neutral Theory, slightly deleterious mutations can persist for hundreds of generations and can even become fixed in the population. It depends on the strength of negative selection (i.e. the selection coefficient) and the size of the population. In small populations, slightly deleterious alleles are invisible to selection and their frequency is entirely controlled random genetic drift.

January 22, 2012
The Modern Molecular Clock
All modern species appear to be at the ends of lineages that have evolved at a relatively constant rate since they diverged from a common ancestor. This result was surprising since most biochemists thought of evolution by natural selection as the main mechanism. How is it possible that the environments of insects, yeast, and primates change at a constant rate causing natural selection to make the same number of changes in each lineage over millions of years?

The same result was observed when bacteria were added to the tree a few years later. There's an approximate molecular clock. Of course by that time Kimura and others (including Fitch) had published on Neutral Theory and that explained the approximate molecular clock. The changes in amino acid sequence are neutral and they become fixed by random genetic drift. Since drift is a stochastic process, the rate of fixation of these neutral alleles is approximately constant over time.1 The astonishing conclusion—which most people still don't grasp—is that the vast majority of all evolutionary change is by random genetic drift, not natural selection.

January 23, 2012
What's the Difference Between a Human and Chimpanzee?
The number of differences between the human and chimpanzee genomes is consistent with Neutral Theory and fixation by random genetic drift.

March 22, 2012
Human Mutation Rates May Be Lower than We Thought
I don't understand all the mathematical manipulations but they are probably trustworthy. (Some of it was done by Reed Cartwright of Panda's Thumb.) The final estimates are 60 mutations in one of the children and 50 in the other. Both of these values are lower than the calculated rate and when you combine them with earlier results, it's beginning to look like the actual mutation rate is about half of the calculated value based on biochemistry. This could easily be due to a two-fold error in our estimate of repair efficiency. It could be that instead of repairing only 99/100 sites of damage the actual repair machinery fixes 199/200 damaged sites, for example.

May 7, 2012
The Problem with Philosophy: Elliott Sober
Elliott Sober argues that evolution and religion are compatible because god could have guided evolution by creating specific mutations that scientists could not recognize as "non-random."

August 1, 2012
Our genome is degenerating, but wait, someone is coming to help us
According to plant geneticist, John Sanford, the human race is degenerating rapidly. It's one of the trade secrets of biology. Every population geneticists knows that it's true.

Sanford has even written a book about this trade secret: Genetic Entropy and the Mystery of the Genome

Now if humans are degenerating at the rate of 1% or so per year then this must mean that they were perfect only a short time ago—like maybe 6000 years?

August 11, 2012
Is "Unguided" Part of Modern Evolutionary Theory?
Modern evolutionary theory consists of many parts including the mechanisms of evolution. The main mechanisms are natural selection and random genetic drift and those two mechanisms act on populations containing variation. The variation is due to the presence of mutations and mutations arise "randomly" with respect to ultimate purpose or goal.

There are tons of experiments proving that mutations are essentially random. (Let's not get into quibbling about the meaning of "random.")

August 13, 2012
An Example of "Directed" Mutation and an Idiotic "Gotcha"
But this isn't the only form of counter-attack. Creationists also like to argue that mutations are not truly random. They point out that there are mutational hotspots in the genome and there's a bias in favor of some mutations over other (e.g. transitions are more common than transversions). In most genomes, mutations are more common at sites where C is methylated.

All this is true and the results were discovered by scientists, not creationists. It's why scientists try to avoid saying that mutations are random; instead they say that mutations are random with respect to their ultimate usefulness.

August 22, 2012
Tomoko Ohta and Nearly Neutral Theory
It's very important to understand the essence of Nearly Neutral Theory since it explains the relationship between fitness and population size. Everyone needs to understand that Ohta demonstrated how slightly deleterious alleles can be fixed in a population. Her work showed that an allele can become effectively neutral in small populations even though it may actually lower the fitness of an individual. It's a way of explaining the limits of natural selection and of extending the Neutral Theory of Kimura.

November 18, 2012
The Most Spectacular Mutation in Recent Human History
Benjamin Phelan is a writer. He has an article in Slate on The Most Spectacular Mutation in Recent Human History.

I'm not going to tell you what it is. You'll have to read his article. But here are a few hints.

November 18, 2012
Ann Gauger Says Random Mutation Can't Possibly Account for Observed Evolution
The Intelligent Design Creationists change their stories so often that it's sometimes hard to keep up. The latest rationalization has to do with the sufficiency of random mutations. Here's the version given by Ann Gauger, Senior Research Scientist at Biologic Institute.

November 22, 2012
Breaking News: IDiots Don't Understand Genomes or Biology
Creationists at the Discovery Institute demonstrate that they don't understand mutation. They are surprised to learn that the genomes of different cells in our body are not 100% identical!

February 1, 2013
What Is a Mutation?
"In genetics, a mutation is a change of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element. Mutations result from unrepaired damage to DNA or to RNA genomes (typically caused by radiation or chemical mutagens), from errors in the process of replication, or from the insertion or deletion of segments of DNA by mobile genetic elements.[1][2][3] Mutations may or may not produce discernable changes in the observable characteristics (phenotype) of an organism."

March 18, 2013
Estimating Human the Human Mutation Rate: Biochemical Method
Adding these together gives us about 133 new mutations in every zygote. Let's round this off to 130. Thus the estimate from the Biochemical Method is .. 130 mutations per generation

March 20, 2013
Estimating the Human Mutation Rate: Phylogenetic Method
"The phylogenetic method relies on a known phylogenetic tree to pick out close relatives and the approximate time to the last common ancestor. In the case of humans, we know that chimpanzees and bonobos are our closest cousins and we think that the homind line diverged from the chimp line about 5 million years ago."

March 22, 2013
Estimating the Human Mutation Rate: Direct Method
"The Direct Method involves sequencing the entire genomes of related individuals (e.g. mother, father, child) and simply counting the new mutations in the offspring. You might think that the Direct Method gives a definitive result that doesn't rely on any assumptions, therefore it should yield the most accurate result. The other two methods should be irrelevant."

May 3, 2013
The Molecular Evolution Exam
"Imagine that identical female twins were born to a woman in 1000 AD. Imagine that you could find a direct descendant of each twin in 2013. If you sequence the complete genomes of the descendants, approximately how many differences would you expect to find?"

June 1, 2013
Mutation-Driven Evolution
"I just learned that Masatoshi Nei is about to publish a new book called Mutation-Driven Evolution."


John Harshman said...

That was a great service to the reader, or at least to this reader, as I hadn't read all of those. Thanks.

Piotr Gąsiorowski said...

Seconded. It's practically a handbook.

Dov Henis said...

Update religious AAAS biology concepts...

Random Biological Mutations Are Impossible

Randomness is impossible in an evolving system:

Random Biological Mutations Are Impossible since biology is an evolving sub-system in the evolving universe system.

All the sub-systems in the universe are CONTINUOUSLY evolving, driven-oriented-directed by the natural selection of ALL mass formats, which is the enhancing of their energy constraint, to temporarily postpone their reconversion to energy, which goes on at constant rate since the Big Bang.

Ponder/re-comprehend non-religious biology,

Dov Henis (comments from 22nd century)
From non-religious Biology:
The Genome is a base organism evolved, and continuously modified, by the genes - the elementary life organisms - of its higher organism as their functional template. DH

Unknown said...