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Wednesday, April 18, 2012

The Problem of Evolution in America

Once again, Jerry Coyne gets it right.1 He is about to publish an article in the journal Evolution on Science, Religion, and Society: The Problem of Evolution in America. There's a link from his blog [My paper on religious and social factors affecting American acceptance of evolution] where he notes that the manuscript isn't quite ready for publication and most of you can't see it because it's behind a paywall.

Here's the abstract ...
American resistance to accepting evolution is uniquely high among First World countries. This is due largely to the extreme religiosity of the U.S., which is much higher than that of comparably advanced nations, and to the resistance of many religious people to the facts and implications of evolution. The prevalence of religious belief in the U.S. suggests that outreach by scientists alone will not have a huge effect in increasing the acceptance of evolution, nor will the strategy of trying to convince the faithful that evolution is compatible with their religion. Since creationism is a symptom of religion, another strategy to promote evolution involves loosening the grip of faith on America. This is easier said than done, for recent sociological surveys show that religion is highly correlated with the dysfunctionality of a society, and various measures of societal health show that the U.S. is one of the most socially dysfunctional First World countries. Widespread acceptance of evolution in America, then, may have to await profound social change.
Sandwalk readers will be familiar with Coyne's attack on accommodationism because he's absolutely correct. You will also understand that the problem is not evolution vs creationism but science vs religion. You can't ever solve the problem of creationism without dealing directly with the false doctrines of religion.

But Coyne goes one step further. How do you make America into a more secular society like those in other Western industrialized nations? Coyne argues that the popularity of religion in America is due to the fact that America is a dysfunctional society and religion may represent the only hope most people have in such a society. Therefore ...

Creationism in America, then, may be a symptom of religion, but religion in the modern world may itself be a symptom of unhealthy societies. Ultimately, the best strategy to make Americans more receptive to evolution might require loosening the grip of religion on our country. This may sound not only invidious but untenable, yet data from other countries suggest that such secularism is possible and, indeed, is occurring in the United States right now. But weakening religion may itself require other, more profound changes: creating a society that is more just, more caring, more egalitarian. Regardless of how you feel about religion, that is surely a goal most of us can endorse.
I think he's right about this. You can remove the need for religion by creating a more just society. But I don't think it will be easy. Looking at it from the outside, it appears to me that there are millions of Americans who don't accept the just society2 as a desirable goal. They call themselves "Republicans" and they vote for people like Rick Santorum.

I think it's also going to be very difficult to convince most Americans that their society is less than perfect. In other words, most of the rest of American society accepts the concept of a just society but firmly believes that America is the only country that has achieved it.


1. That doesn't mean that he's right all the time. It just means that his batting average is way above average for an evolution defender.

2. Canadians will be familiar with the term since the just society was the goal of Prime Minister Pierre Elliot Trudeau who named his son, and political heir, "Justin."

Tuesday, April 17, 2012

Dysfunctional Science

Carl Zimmer, one of the top science writers in the world, has written an article for the New York Times with the following provocative title: A Sharp Rise in Retractions Prompts Calls for Reform. It's partly about the rise in the rate of retractions1 in scientific journals. This is a serious problem and it's hard to figure out the underlying cause, in spite of the fact that many of the people who comment think they know the answer.

But there's much more to this story as Carl explains on his blog [Dysfunctional science: My story in tomorrow’s New York Times].
In tomorrow’s New York Times, I’ve got a long story about a growing sense among scientists that science itself is getting dysfunctional. For them, the clearest sign of this dysfunction is the growing rate of retractions of scientific papers, either due to errors or due to misconduct. But retractions represent just the most obvious symptom of deep institutional problems with how science is done these days–how projects get funded, how scientists find jobs, and how they keep labs up and running.
As usual, Carl's got it right. There's something wrong with science, or perhaps I should say there's something wrong with the biological sciences since Sean Carroll doesn't see the same problem in physics [Is Physics Among the Dysfunctional Sciences?].


1. The rate is about 0.04%. Compare this to the rate of fraudulent creationist publications, which is close to 100%.

Monday, April 16, 2012

Monday's Molecule #166

This is another one of those molecules where you have to pay close attention to the structure. There are many similar molecules and you won't win unless you are very specific. You don't need the full IUPAC name. You do need to identify the function of this molecule.

Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answers wins. I will only post correct answers to avoid embarrassment. The winner will be treated to a free lunch.

There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date.

Comments are invisible for 24 hours. Comments are now open.

UPDATE: The molecule is heme a, a component of cytochrome a and cytochrome a3. The cytochromes are cofactors in oxidation-reduction reactions where the heme group serves as an electron donor or acceptor. Today's winner is Raul A. Félix de Sousa. Several anonymous/pseudoanonymous respondants were also correct.

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout
April 9: no winner
April 16: Raul A. Félix de Sousa


Sunday, April 15, 2012

The Myth of "Living Fossils"

The general public has been told time and time again that there exist among us certain species that have not evolved for millions of years. These so-called "living fossils" have somehow managed to avoid any changes in the frequencies of alleles in their evolving populations. This is, of course, impossible by any reasonable definition of evolution, a conclusion that was promoted on talk.origins two decades ago [Claim CB930:].

Yet the myth persists. It persists for three reasons:
  1. It plays into the popular misconception that natural selection is synonymous with evolution. If a species isn't adapting by obvious changes over time then it isn't evolving. Another way of saying this is that some species can be so perfectly adapted to their environment that all changes are selected against and negative selection prevents evolution.
  2. External morphological changes are the only evidence of evolution.
  3. The so-called "living fossils" show no evidence of morphological change over millions of years when, in fact, all of the popular examples show plenty of evidence of such change. In other words, the facts are misrepresented.
The last time I blogged about this was just a few months ago when I commented on the first episode of a BBC television documentary called "Survivors." The main topic of the first episode was "Horseshoe crabs are one of nature’s great survivors" and the scientist behind the series is Richard Fortey, a paleontologists at the Natural History Museum in London (UK). I pointed out that some of his statements were misleading and I also explained why horseshoe crabs have evolved according to the scientific evidence [Evolution of Horseshoe crabs].

Why is this important? Because it's wrong to promote incorrect versions of evolutionary theory.

Today's New York Times Book Review has a review of a new book by Richard Fortey called "Horseshoe Crabs and Velvet Worms." The review [Some Things Should Be Dead] praises the writing style and readability of the book but, like most science journalism, does not get into details about the accuracy of the text.1

While preparing this post, I discovered that Jerry Coyne had also read the review [Two New Biology Books]. Coyne has met Fortey and thinks him a "lovable bear of a man, infectiously excited about biology." However, Coyne wonders what explanation Fortey will offer to support his claim of fossil species.
Fortey has a new book, and it’s about “living fossils,” those plants and animals that have persisted for millions of years without much change in their morphology (think ginkgo tree, coelocanth, and horseshoe crab). To evolutionists, these species are a mystery: why have they remained unchanged so long? One explanation—that they simply lack genetic variation that fuels evolution—is probably wrong: work ages ago by Bob Selander and Dick Lewontin showed that horseshoe crabs are just as genetically variable in their DNA as more malleable species. Another classic explanation is that these species simply live in unchanging environments, so that they arrived at their optimal morphology eons ago and there’s nothing new to adapt to. That’s an appealing but largely untestable explanation, especially because some creatures that live in similar habitats (like the shallow marine habitats of the horseshoe crab) have undergone substantial evolutionary change.

At any rate, Fortey’s new book is "Horseshoe Crabs and Velvet Worms: The Story of the Animals and Plants that Time has Left Behind," and it was reviewed in Thursday’s NYT. Reviewer Dwight Garner gives it two thumbs up, and I’ll be reading it for sure, if for no other reason to see Fortey’s explanation for unchanging species.
I'm not going to buy the book 'cause the only explanation I could accept would be that there's no such thing as a living fossil. I might be interested in a lengthy discussion about the different between natural selection and random genetic drift and/or a discussion about the kinds of morphological changes that have been observed recently among the four living species of horseshoe crabs but I doubt that would be in Fortey's book. Maybe Jerry Coyne will read it and prove me wrong.


1. This is a pet peeve of mine. The top three most important criteria of good science writing are: accuracy, accuracy, and accuracy. If a review doesn't tell me about the quality of science in a book then the review is completely useless. I don't care if the book wins a Pulitzer Prize (given out by non-scientists) for being an enjoyable read that sounds convincing to most readers. I don't judge science writing by style as the first criterion, nor do I judge it by the personality of the writer.

Friday, April 13, 2012

Teaching Evolution in Tennessee


The state of Tennessee is about to have a new law that impacts the teaching of science in their public schools. Here's how the National Center for Science Education (NCSE) describes the law.
Nicknamed the "monkey bill," HB 368 would, if enacted, encourage teachers to present the "scientific strengths and scientific weaknesses" of topics that arouse "debate and disputation" such as "biological evolution, the chemical origins of life, global warming, and human cloning."
It doesn't take a mental giant to see where the Tennessee legislators are coming from. They want to support teachers who challenge evolution in the classroom. Most of those teachers will, of course, be creationists of one form or another.

But here's the problem. Those ignorant legislators have been very clever to avoid mentioning religion or creationism. On the surface, the new law looks perfectly reasonable.After all, who wouldn't want students to learn both the scientific strengths and weaknesses of current theories of biological evolution?

Monday, April 09, 2012

Winners

Here are three winners having lunch. On the left is David Schuller (Monday's Molecule #156) and that's Joseph Somody (Monday's Molecule #159) on the right.

(Thank-you David for the photo.)


Monday's Molecule #`165

Name this molecule. You don't need the full IUPAC name but you do need to be specific since there are several different molecules with very similar structures. You also have to tell us why this molecule is important in biochemistry.

Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answers wins. I will only post correct answers to avoid embarrassment. The winner will be treated to a free lunch.

There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date.

Comments are invisible for 24 hours. Comments are now open.

UPDATE: The Molecule is kanamycin C (not A or B). It binds to the small subunit of the prokaryotic ribosome and inhibits translation. It is/was widely used in cloning experiments since there are several plasmids with kanamycin resistance alleles. I posted all three of the responses that recognized kanamycin but only one named this variant as kanamycin C. That person didn't mention that this was a translation inhibitor so there are no winners this week.

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout
April 10: no winner


Thursday, April 05, 2012

The Toronto Transit Commission Stands for Freedom of Speech

The Toronto Transit Commission (TTC) has resisted attempts to have a controversial ad removed from their buses, streetcars, and subways as reported in The Toronto Star [TTC won’t remove controversial ads].
But a review that is automatically triggered whenever the TTC gets at least five complaints about an ad found there were no grounds to pull either advertisement.

That review was by TTC chair Karen Stintz and TTC commissioner Maria Augimeri.

“Although I would not personally condone the comportment outlined in the advertisement, I feel that I do not have the jurisdiction nor the authority to promote its cancellation; particularly because the TTC would not fare well in a court challenge should the promoter of the advertisement choose to make this issue one of rights and freedoms,” Augimeri said of the ... ad.

“There is nothing that violates any of our policies, and we do have policies around our advertising (based on) the Ontario Human Rights Code, not promoting hate or violence,” said TTC spokesman Brad Ross.

“You don’t have to agree with the message, you don’t have to like the message of the advertiser. Our suggestion would be that if somebody takes issue with the ad they take it up with the advertiser,” he said.
Congratulations TTC! That's exactly right.

It doesn't matter what sort of ad triggered the complaints but just in case you're interested, here it is. The first paragraph says, "Dear Jesus, My mom and dad do drugs at home and it scares me. Will you help them stop? Thank you for hearing my prayer." The second paragraph is, "Don’t worry about anything; instead, pray about everything. Tell God what you need, and thank him for all he has done. If you do this you will experience God’s peace, which is far more wonderful than the human mind can understand." The ad is sponsored by Bus Stop Bible Studies.


Note: Hemant Mehta has a slightly different take on the issue [Christian Bus Ad Advises Child with Druggie Parents to Pray, Not Call for Help].


[Hat Tip: Canadian Atheist]

Tuesday, April 03, 2012

Evo Devo and Giants

Anything found to be true of E. coli must also be true of elephants.

-Jacques Monod (1954)
While preparing for the last lecture in my molecular evolution course I came across this quotation that explains Evo Devo.
The key to understanding form is development, the process through which a single-celled egg gives rise to a complex, multi-billion-celled animal. This amazing spectacle stood as one of the great unsolved mysteries of biology for nearly two centuries. And development is intimately connected to evolution because it is through changes in embryos that changes in form arise. Over the past two decades, a new revolution has unfolded in biology. Advances in developmental biology and evolutionary developmental biology (dubbed “Evo Devo”) have revealed a great deal about the invisible genes and some simple rules that shape animal form and function. Much of what we have learned has been so stunning and unexpected that it has profoundly reshaped our picture of how evolution works. Not a single biologist, for example, ever anticipated that the same genes that control the making of an insect’s body and organs also control the making of our bodies.

Sean B. Carroll “Endless Forms Most Beautiful: The New Science of Evo Devo” W.W. Norton & Co., New York (2005)
I've already criticized this point of view several times [Things You Didn't Know] [Sean Carroll's View of Evo-Devo] and I won't repeat them here. Read those posts to see what's wrong with Evo Devo.

If I have seen further it is by standing on ye sholders of Giants.

Isaac Newton, 1676
I want to emphasize another point. I come from a culture that praised and admired the important work that formed the background to modern discoveries. My mentors were proud of the fact that they stood on the shoulders of giants.

Someone named anthrosciguy commented on my earlier post [Sean Carroll's View of Evo-Devo] by saying ...
No one wants to stand on the shoulders of giants anymore.
That struck me as a profound commentary on much of modern biological science so I thought I'd share it with you. These days it seems like everyone wants to claim credit for discovering something that nobody anticipated. You can't be standing on the shoulders of giants if you're proclaiming a revolution. That would look silly.

I'm pretty sure I know anthrosciguy's real identity but I'll leave it to him to out himself and take credit for a very clever statement.


Monday, April 02, 2012

Carnival of Evolution #46

 
This month's Carnival of Evolution (46th version) is hosted by Bradly Alicea of Synthetic Daisies: Carnival of Evolution, Number 46 -- The Tree (structures) of Life
Welcome to Carnival of Evolution, Number 46. I am your host, Bradly Alicea. This month's theme is: the Tree (structures) of Life. Since this blog covers a mix of both biological and computational content, it is fitting that we explore this month's submissions in the context of trees (the computational kind) and biological classification (the biological kind). I will indulge in a historical and technical overview of trees used in evolutionary analysis, then present this month's posts.

The next Carnival of Evolution (May) will be hosted by John Wilkins and the one after that by PZ Myers. You can send articles directly to them or you can submit your articles at Carnival of Evolution. Bjørn is looking for someone to host the July edition. He would prefer someone who has not hosted before. Contact him at the Carnival of Evolution blog.


Monday's Molecule #164

 
What is this structure and what is its significance? You don't need to come up with a chemical name but you do need to be as specific as possible.

Don't forget to tell us why this structure exists.

Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answers wins. I will only post correct answers to avoid embarrassment. The winner will be treated to a free lunch.

There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date.

Comments are invisible for 24 hours. Comments are now open.

UPDATE: The molecule is the cap structure on the 5′ end of eukaryotic mRNAs. It's actually a CAP 2 structure with methyl groups at the 2′ positions of the last two nucleotides but that terminology seems to be outdated so I won't insist that you specify. (Thanks to Bill Chaney for getting it right.) The winner is Sean Ridout. (Please contact me by email.)

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout


Thursday, March 29, 2012

Food Trucks

 
I love the food trucks. Today was a special day, there were seven new food trucks visiting our campus.


There were so many choices ....


Two of my favorites ...



Bacon poutine and a cinnamon-sugar BeaverTail. Only in Canada!



The Reason Rally

 
For all of us who weren't there, here's what The Thinking Atheist saw at the Reason Rally last weekend.



Monday, March 26, 2012

Monday's Molecule #163

 
You blew it last week because you didn't follow instructions. It's not going to get any easier. This week you have to identify the molecule using TWO different common names AND name the Nobel Prize winner most closely associated with this molecule.

Remember, you need THREE answers or you can't win!

Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answers wins. I will only post correct answers to avoid embarrassment. The winner will be treated to a free lunch.

There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date.

Comments are invisible for 24 hours. Comments are now open.

UPDATE: The molecule is Vitamin B12, also known as cobalamin. The Nobel Laureate is Dorothy Crowfoot Hodgkin. This week's winners are John Runnels and Raul A. Félix de Sousa. Contact me by email to set up a time.

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner


Thursday, March 22, 2012

Human Mutation Rates May Be Lower than We Thought

The predicted mutation rate in humans is thought to be about 130 mutations per generation or 10-10 per nucleotide per generation [Mutation Rates]. About 120 (>90%)of these new mutations occur in males, mostly during spermatogenesis. Only about 10 mutations are contributed by females. These values are based on what we know about the biochemistry of DNA replication and repair.

The evidence from evolution was consistent with this calculation. Nachman and Crowell (2000), for example, calculated that the accumulation of mutations in 18 pseudogenes from humans and chimpanzees yielded a value of 175 mutations per generation.

Up until recently it wasn't possible to get a direct measurement of the mutation rate but I addressed some of the attempts in November 2010: Human Mutation Rates. In that posting I discussed two experimental results that yielded estimates of the mutation rates in humans.
Recently there have been two attempts to verify this calculation. In one, the Y chromosomes of two men separated by 13 generations in a paternal lineage from a common male ancestor were sequenced. The differences correspond to a mutation rate of 0.75 × 10-10 per generation, or almost the same as theory predicts. This is based on the fact that if most mutations are nearly neutral (they are) then the rate of fixation by random genetic drift should be the same as the mutation rate.

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. 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.
Now there's another paper that sequenced two sets of parents and a child (Conrad et al., 2011). You might think that the calculation is easy because all you have to do is count the number of new alleles in the child. But this doesn't work because you have to account for somatic mutations that arose in the tissue culture cells lines that are being used as a source of DNA. These can be eliminated by comparing the sequence with fresh DNA samples directly from the parents and child. In addition to false positives, you have to allow for some false negatives.

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.

The surprising result is that 92% of the new mutations in one of the children comes from the father but in the other family only 32% of the mutations were paternal. We expect that most of the mutations will occur during spermatogenesis so that part is not surprising. What's surprising is that in one case the majority come from the mother.

I suspect that this is an artifact of some kind, or a statistical outlier. The authors, however, take this as evidence of natural variation in male and female mutation rates. I'd like to see the estimates for other children of the same family in order to see if the result is reproducible.


Conrad, D.F., Keebler, J.E., DePristo, M.A., Lindsay, S.J., Zhang, Y., Casals, F., Idaghdour, Y., Hartl, C.L., Torroja, C., Garimella, K.V., Zilversmit, M., Cartwright, R., Rouleau, G.A., Daly, M., Stone, E.A., Hurles, M.E., Awadalla, P.; 1000 Genomes Project. (2011) Variation in genome-wide mutation rates within and between human families. Nat. Genet. 43:712-714. [doi: 10.1038/ng.862]

Nachman, M.W. and Crowell, S.L. (2000) Estimate of the mutation rate per nucleotide in humans. Genetics: 156:297-304.