A couple of years ago I posted an article on How Did the Zebra Get Its Stripes?.
I pointed out that this wasn't a Rudyard Kipling story but that many of the explanations had strong ties to just-so stories. I noted that everyone just assumed that there had to be an adaptive explanation for zebra stripes so they kept looking and looking. Every time one of the adaptive explanations was ruled out, they invented another one.
The best explanation back in 2012 was that zebra stripes evolved to protect zebras from horseflies and there was some experimental support for the idea that horseflies tended to avoid stripes. However, there was no evidence that avoiding some horseflies actually conferred enough selective advantage to drive the evolution of stripes.
Now we have a press release that announces the final solution: Scientists solve the riddle of zebras' stripes.
Why zebras have black and white stripes is a question that has intrigued scientists and spectators for centuries. A research team led by the University of California, Davis, has now examined this riddle systematically. Their answer is published April 1 in the online journal Nature Communications.
The scientists found that biting flies, including horseflies and tsetse flies, are the evolutionary driver for zebra's stripes. Experimental work had previously shown that such flies tend to avoid black-and-white striped surfaces, but many other hypotheses for zebra stripes have been proposed since Alfred Russel Wallace and Charles Darwin debated the problem 120 years ago.
Sounds like old news to me. And I'm still not convinced that you need an adaptive explanation.
Here's the paper ...
Caro, T., Izzo, A., Reiner Jr, R.C., Walker, H. and Stankowich, T. (2014) The function of zebra stripes. Nature Communications 5, Article number: 3535 [doi: 10.1038/ncomms4535]
Despite over a century of interest, the function of zebra stripes has never been examined systematically. Here we match variation in striping of equid species and subspecies to geographic range overlap of environmental variables in multifactor models controlling for phylogeny to simultaneously test the five major explanations for this infamous colouration. For subspecies, there are significant associations between our proxy for tabanid biting fly annoyance and most striping measures (facial and neck stripe number, flank and rump striping, leg stripe intensity and shadow striping), and between belly stripe number and tsetse fly distribution, several of which are replicated at the species level. Conversely, there is no consistent support for camouflage, predator avoidance, heat management or social interaction hypotheses. Susceptibility to ectoparasite attack is discussed in relation to short coat hair, disease transmission and blood loss. A solution to the riddle of zebra stripes, discussed by Wallace and Darwin, is at hand.
I'm betting that in five years there will be papers examining the SIX major adaptive explanations and five of them will be ruled out in favor of the latest one.
Although all types of creationists are anti-science to some degree,1 the Intelligent Design Creationists are unusual because they don't just ignore science, they try to use science to show that science is wrong!
When dealing with the similarities between closely related species, they claim that the similarities (and differences) are due to design and not evolution. They claim that evolution cannot account for the differences between, say, humans and chimps. Only intelligent design can do that.
In an attempt2 to show them that evolution CAN account for the differences between humans and chimps/bonobos, I wrote up a description of how Neutral Theory and random genetic drift produce genomes that differ by 22 million positions if we take the fossil evidence at face value and assume that chimps and humans last shared a common ancestor about 5 million years ago [Why are the human and chimpanzee/bonobo genomes so similar?].
Apparently there are some creationists who are slightly embarrassed that they don't understand evolution. First, there was Vincent Torley who made an attempt to understand population genetics (from the 1920s and 1930s) and Neutral Theory, which is only 45 years old. You can read his attempt at: Fixation: the neutral theory’s Achilles’ heel?. See my attempt to correct his errors at: A creationist illustrates the argument from ignorance while trying to understand population genetics and Neutral Theory.
I appear to have been partially successful because if you scroll down to the bottom of Vincent Torley's post you'll see an "update" that pretty much refutes his entire post.
The comments on Torley's post reveal that there are very few creationists who have ever heard of population genetics and Neutral Theory. Now that they've been exposed, their response is to reject it because they don't understand it. Salvador Cordova (scordova) pops up in those comments to explain that modern evolutionary theory is all wrong because of "unfixing." Apparently, evolutionary biologists have missed something important that only creationists can see. This happens a lot.
Sal is so proud of himself that he puts up another post at Uncommon Descent: Fixation rate, what about breaking rate?. One gets the impression that some of the creationists are a bit worried.
The irony is that the vast majority of creationists will have absolutely no idea what Cordova is talking about. To them, it's like he's speaking gibberish. In this case, it means that the average IDiot isn't even posting comments under Cordova's post because they don't know what to say. This is all news to them.
So, what is the great discovery that refutes population genetics and Neutral Theory? It's got something to do with the idea that for neutral alleles the rate of fixation is equal to the mutation rate. Cordova agrees with the math but thinks it is "flawed from a functional standpoint." Why? Because ...
Ok, so let’s do an experiment. Let’s subject bacteria or plants or any organism to radiation and thus increase the mutation rate mutation rate by a factor of 1 million or 1 billion. Do you think the above formula will still hold? We tried it in the lab, it killed the plants, and at some point rather than speeding evolution we are doing sterilization.
Cordova is correct. An organism will die if you subject it to massive amounts of radiation. This blast doesn't have much to do with mutation rate but later on Cordova comes closer to a serious discussion of evolutionary theory.
Here's what upsets him ...
... even with moderate rates of mutation per individual per generation, genetic deterioration will happen. Further, this claim is reinforced by the work of Nobel Prize winner Hermann Muller who said a deleterious mutation rate of even 0.5 per individual per generation would be sufficient to eventually terminate humanity. So the simple model I present is actually more generous than Muller’s. Current estimates of the number of bad mutations are well over 1.0 per human per individual. There could be hundreds, perhaps thousands of bad mutations per individual per generation according to John Sanford. Larry Moran estimates 56-160 mutations per individual per generation. Using Larry’s low figure of 56 and generously granting that only about 11% of those are bad, we end up with 6 bad mutation per individual per generation, 6 times more than the cartoon model presented, and 12 times more than Muller’s figure that ensures the eventual end of the human race.
He's talking about genetic load although he goes out of his way to avoid using that term.
Sal Cordova is correct that if the deleterious mutation rate is too high, the species will go extinct. We don't know the exact minimum number of deleterious mutations that have to happen per generation in order to cause a problem. It's probably less than two (2). It's probably not as low as 0.5. It should be no more than 1 or 2 deleterious mutations per generation.
Genetic load arguments have been around for over forty years [Non-Darwinian Evolution in 1969: The Case for Junk DNA]. Back then, they were used to explain that most of our genome is junk and mutations in that part of the genome have no effect. We now know that those arguments were correct and 90% of our genome is junk.
Imagine that there are 130 new mutations per generation. Since only 10% of our genome is functional DNA, this means that only 13 of these mutations occur in DNA that has a biological function. We know that in a typical coding region about 25% of all mutations are seriously detrimental so if all the functional region of the genome were coding region that would mean 3.25 detrimental mutations per generation.1 However, less than 2% of our genome encodes protein. The remaining functional regions are much less constrained so they can tolerate more mutations. It's likely that there are fewer than 2 detrimental mutations per generation and this is an acceptable genetic load.
All of this information is readily available in textbooks and scientific papers. It's basic evolutionary theory and facts about the human genome.
Cordova is correct to raise the point about genetic load but he is quite wrong in his calculation.
Still, we seem to be making a bit of progress because at least the creationists are talking about evolutionary theory from the 100 years after Darwin died.
Better late than never. Now all they have to do is get the facts right and they'll be ready to move into the 21st century.
Lynch, M. (2010) Rate, molecular spectrum, and consequences of human mutation. Proceedings of the National Academy of Sciences 107, 961-968. [doi: 10.1073/pnas.0912629107]
Keightley, P.D. (2012) Rates and fitness consequences of new mutations in humans. Genetics 190, 295-304. [doi: 10.1534/genetics.111.134668]
Kondrashov, A.S. (2002) Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases. Human mutation 21, 12-27. [doi: 10.1002/humu.10147]
1. Estimates of the percentage of deleterious mutations in coding regions are all over the map. I figure that most distantly related genes are only 30% identical in amino acid sequence. Some mutations in the conserved amino acid codons will be synonymous. But even if this value is 50% instead of 25%, the total number of deleterious mutations in coding regions would only be 50% × 2% × 130 = 1.3 deleterious mutations.
I know I've said this before, but I continue to be astonished at the ignorance of creationists. Those who oppose evolution most vehemently don't understand it in spite of the fact that they are convinced it has to be wrong.
This is most obvious with the Intelligent Design Creationists because they like to use science-sounding jargon to convince us that they know what they are talking about. They claim that they can refute evolutionary biology using scientific evidence. Instead they just reveal their ignorance.
They've been doing it for decades in spite of the fact that many people have tried to educate them. I don't get it.
Recently, I tried to explain how the difference between the chimpanzee and human genomes is consistent with what we know about population genetics, mutation rates, and Neutral Theory. I was aware of the fact that this stuff would all be news to most Intelligent Design Creationists but it was still an opportunity to try, once again, to teach them about modern evolutionary theory.
Last week's molecule [Monday's Molecule #234] was insect juvenile hormone. The winners are Frank Schmidt and Raul Félix de Sousa (still an undergraduate?). They live in foreign countries so they won't be coming to lunch.
This week's molecule (right) is very common. You have to identify the entire molecule including the specific polynucleotide. Emphasis is on the word "specific"—there's only one possibility. I'm betting that there won't be very many correct answers for this one.
Email your answer to me at: Monday's Molecule #235. I'll hold off posting your answers for at least 24 hours. The first one with the correct answer wins. I will only post the names of people with mostly 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 email message.)
God's not dead is a movie that's gaining some notoriety in the USA. Here's a synopsis ...
Present-day college freshman and devout Christian, Josh Wheaton (Shane Harper), finds his faith challenged on his first day of Philosophy class by the dogmatic and argumentative Professor Radisson (Kevin Sorbo). Radisson assigns him a daunting task: if Josh will not admit that "God Is Dead," he must prove God's existence by presenting well-researched, intellectual arguments and evidence over the course of the semester, and engage Radisson in a head-to-head debate in front of the class. GOD'S NOT DEAD weaves together multiple stories of faith, doubt and disbelief, culminating in a dramatic call to action.
I haven't seen the movie (yet) but I'm guessing that the 18 year-old Christian student wins the debate against his "dogmatic" professor.
This sort of thing happens quite a bit in the movies. It's pretty rare to find a university professor portrayed as a good person, or even a smart person who knows their stuff. If you are one of those university students who watch the movie and are convinced that you can win a debate with a professor on the subject "Do gods exist?" then please contact me and we'll set up a time and place for you to make the attempt. I'm pretty sure I can find a smart professor at most major universities.
Yesterday afternoon I attended a forum on Science and Mathematics teaching in Ontario schools. It was put on by The Centre for Science, Mathematics and Technology (SMT) Education at the Ontario Institute for Studies in Education (OISE) at the University of Toronto (Toronto, Canada).
OISE is one of the places responsible for training teachers in Ontario. It offers advanced degrees (Masters. Ph.D.) in education. I thought this might be a good opportunity to network with the people responsible for teaching science in our high schools.
Here's a description of the forum ...
The Canadian Secular Alliance is hosting a talk by Lauren Forbes tomorrow evening in rm 4171 of the Medical Sciences Building at the University of Toronto. (My building, one floor below my office.) Contact me if you want to meet up before the talk.
It's important to note that Ms. Forbes is going to DEFEND things like prayer at city council meetings. Come out and hear the other side of the issue. She is a Master's student at the University of Ottawa.
Read her article: To Pray or Not to Pray, is that the Question?: How the Increasing Desire for State Neutrality Affects Prayer Before Council Meetings in Canada. Here's the abstract ...
Historically, in western liberal democratic states, Christian prayers have often been recited at the opening of various public institutions' meetings. However, the recitation of such prayers is now being questioned on the grounds of being too particular in promoting specific religious denominations; of promoting a particular religion over another; and even of promoting religion in states where no longer everyone subscribes to one. Many such disputes spring from the growing desire for equality and neutrality in increasingly diverse and secular societies. This paper focuses on the recent legal disputes in Canada, concerning the recitation of prayers before the commencement of primarily council meetings. It examines Canadian tenets of neutrality and consequently secularism, questioning what each looks like (or could look like) and whether they require public spaces to be religion-free in order to hold true, or whether they can be inclusive to both religious and worldviews of non-belief in these public spaces (i. e. council meetings in this context). In this paper the relevant legal cases are analyzed and current solutions to the disputes are discussed. Concerns are raised and finally, solutions that may be more neutral and that equally do justice to both freedom of religion and freedom of conscience are considered.
I stole this from Ms. Sandwalk's blog. I'm pretty sure she'll mind.
Several students in my class decided to write essays on epigenetics. This was very brave of them since nobody seems to have a good definition of epigenetics and much of the hype about epigenetics is not very scientific. I'm also more than a little skeptical about some of the claims that have been made.
Here's a video. What do you think? Is this a useful contribution to our understanding of a complex issue? Is the inheritance of methylation sites at restriction/modification loci in bacteria an example of epigenetics? After E. coli divides, both cells inherit some lac repressor molecules and the lac operon is not expressed provided the parent wasn't exposed to lactose. Is this epigenetics?
Last week's molecules [Monday's Molecule #233] were oxaloacetate, ethanol, lactate, alanine, and acetyl-CoA. All of them can be synthesized in a reaction using pyruvate as a substrate (two steps to make ethanol). All of them are precursors to pyruvate and hence glucose. The winner is Jean-Marc Neuhaus. I will be buying him four meals next time I visit Switzerland. I'm thinking it will be two raclettes and two fondues with lots of wine.
This week's molecule (left) is probably not very familiar to most of you so I don't anticipate many correct answers. You can use the common name. Email your answer to me at: Monday's Molecule #234. I'll hold off posting your answers for at least 24 hours. The first one with the correct answer wins. I will only post the names of people with mostly 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 email message.)
Today is the 40th anniversary of my Ph.D. oral defense.1 The event took place in the Department of Biochemical Sciences at Princeton University back in 1974.
It began with a departmental seminar. When the seminar was over I retired with my committee to a small classroom for the oral exam.
I don't remember everyone who was on my committee. My Ph.D. supervisor (Bruce Alberts) was there, as was my second reader, Abe Worcel. I know Uli Laemmli was there and so was Arnie Levine. I'm pretty sure the external member of the committee was Nancy Nossal from NIH in Bethesda, MD (USA). It's a bit of a blur after all these years.
I remember being fairly confident about the exam. After five and a half years I was pretty sure that everyone on my committee wanted to get rid of me and the easiest way to do that was to let me pass. Bruce stood to gain $3000 per year of research money and Uli was going to get back the basement of his house where Ms. Sandwalk and I had been living for the past month.
The toughest questions were from Uli Laemmli, which should not come as a surprise to anyone who knows him. He has this annoying habit of expecting people to understand the basic physics and chemistry behind the biochemical sciences. Fortunately, my inability to answer most of his questions didn't deter him from voting to pass me.
This photograph was taken at a party that evening. I look pretty calm at that point but this may have had a lot to do with the various refreshments that were being served.
The amazing thing about the photograph—as I'm sure you all agree—is how little I've changed since then—apart from a haircut.
Back in those days we didn't spend a lot of time writing a thesis. I started in the middle of January and the entire process of writing and defending took nine weeks. My thesis was bound and delivered to the library about one week after the Ph.D. oral.
The second page of my thesis has only three words on it. It says, "To Leslie Jane." This is Ms. Sandwalk. She really should have her name on the cover 'cause I couldn't have graduated without her. Typing my thesis was only one of her many contributions. There are 257 pages in my thesis and she typed every one. As a matter of fact, she typed them twice, one draft and then the final version.
The figures in my thesis were all hand drawn. I've included one (below) to illustrate what I was doing during those five and a half years.
The Alberts lab was interested in DNA replication during bacteriophage T4 infections of E. coli. We knew that replication was carried out by a complex protein machine that assembled at a replication fork but we didn't know all the players or what they did.
The T4 proteins required for DNA replication were known from genetic studies. The most important genes were genes 30 (ligase), 32 (single-stand DNA binding protein), 41, 43 (DNA polymerase), 44, 45, and 62. The products of the unknown genes were called 41P, 44P, 45P and 62P.
We wanted to purify and characterize those proteins; my target was the product of gene 41, or 41P.
We had a cool assay, developed mostly by a postdoc in the lab named Jack Berry. What we did was to prepare a cell lysate from cells that had been infected by bacteriophage carrying an amber mutation in one of the genes. This lysate could not support DNA synthesis, as measured by incorporation of 32P nucleotides, unless we added back the missing component. This is the basis of an in vitro complementation assay that worked for each of the unknown proteins.
In my case, I used traditional protein purification methods to isolate fractions of proteins and them tested them for activity in the complementation assay. The figure below shows the elution profile of proteins bound to a hydroxylapatite column. The peak centered on fraction 61 is the activity of the complementation assay. It indicates that 41P elutes early as a sharp peak in the elution profile.
The complementation assay doesn't tell us anything about the function of 41-protein, only that it complements an extract that's deficient in 41P. Strictly speaking, it doesn't even tell us that the activity is due to the product of gene 41 since it could be something else that complements in vitro.
Fortunately we had another way of identifying 41P. I started my purification with extracts from 17 liters of infected cells. To this I added extracts from cells that had been labeled with radiaoctive amino acids. One batch was from a wild-type infection where all T4 proteins are labeled with 14C amino acids. The other batch is from an infection with an amber mutation in gene 41. In this case every protein except 41P is labeled with 3H amino acids.
You can adjust the settings on a scintillation counter so they distinguish between 14C and 3H but there's some overlap. The equations for calculating the contribution of each isotope in each window are relatively simple. All you need are good standards to get the distribution. One of the most fun things I did as a graduate student was to write a computer program (in Fortran) that did these calculations automatically and plotted them on a plotter. This was back in the time when computers were housed in large separate buildings and required dozens of people to look after them.
If you look of the elution profile in the figure you'll see there's an excess of 14C over 3H in the same fractions where the complementation activity is located. What this means is that the wild-type extract has a protein at that position that's not found in the am41 extract. It's another way of identifying the product of gene 41.
The double label technique was useful 35 years ago but nobody does it anymore. It was fun while it lasted.
(I never did figure out what 41P did during DNA replication but a few years after I left a postdoc identified 41P as a helicase—an enzyme that unwinds DNA ahead of the replication fork. The enzyme is now called gp41 for "gene product.")
1. This post is an almost identical copy of one that was posted five years ago. You'll probably see another in 2019, and especially 2024.
The genomes of chimpanzees and bonobos are remarkably similar to the human genome. In terms of sequence similarity, they are more than 98% identical in the regions that can be aligned. This, of course, is due to the fact that they descend from a common ancestor in the recent past (about 5 million years ago).
Intelligent Design Creationists don't agree. Many of them do not accent common descent and macroevolution so they make up stories that account for the similarity based on what they think god might have been thinking when he created chimps and humans.
But the scientific evidence for evolution is much stronger than just overall sequence similarity. The number of differences (about 50 million substitutions) corresponds pretty closely with what we expect from evolutionary theory (population genetics) and known mutation rates [Why are the human and chimpanzee/bonobo genomes so similar?]. If the Intelligent Design Creationists are going to dismiss this confirmation of evolutionary theory then they are going to have to be much more inventive.
John Wilkins has written a series of posts about the war between science and religion.
Accommodating Science overview
I find the arguments confusing because I'm never quite sure what John defines as "science." I think he's referring to the things that scientists do. This is the narrow definition of science and I think it explains why he claims that there are aspects of religion that do not conflict with science.
