This YouTube video is described as "The most ignorant 82 seconds you'll ever see." I don't know about that. I been around IDiots for quite a long time. It may not be the "most ignorant" but it's surely in the top ten.
Remember, this is the best they've got. Really. Trust me on this.
Today is the last day of classes at the University of Toronto and I have to submit a copy of the final exam to the Examination Supervisor. Actually, I have to submit a copy for each student PLUS 11 extra copies AND the "original." They have to be in two separate sealed packages with specified labels on the outside.
There's a set of rules and regulations that must be followed, including specific formatting rules. Some of the rules make sense and some don't.
Rule #12 is interesting. Here's what it says ...
Instructors and departmental offices should take stringent measures to prevent unauthorized persons from having access to the examinations. NO COPY OF AN EXAMINATION IS TO BE KEPT IN THE DEPARTMENT BEFORE THE FINAL EXAMINATION IS WRITTEN. This applies to electronic storage as well as to flash drives/usb key and paper copies.
Those of you who know me well will be able to imagine how much effort I have taken to erase everything from my hard drive and the automated backup drive attached to my computers. They will understand exactly how difficult it was for me to check my flash drive to make sure that no copy of the exam was stored there or in dropbox. They'll also know just how scrupulous I've been about not having a copy of my exam anywhere in my files. They can imagine that I've stored a copy safely at home so I can print out a version the day after the exam is written and put if back on my desktop hard drive.
I wonder how many of my colleagues will follow this rule? What do you think the penalty is if you don't?
Thank the gods for bureaucrats.
The President of the University of Toronto recently published an article about undergraduate education. I questioned whether my university really is committed to the ideals of undergraduate education (critical thinking etc.) [Does the University of Toronto really care about undergraduate education?]. The answer, IMHO, is "no."
Now I want to bring up something else from the article by President Meric Gertler. It's not a major point—more like a motherhood throwaway line—but I think it raises an interesting question. Gertler said,
U of T reaffirms the value of a broad liberal arts education at the undergraduate level, and we are working to help our graduates extract the full benefit from that education.
I suppose there are as many definitions of "liberal arts education" as there are teachers but I think we can agree on a few points. A "liberal arts education" does not put much emphasis on math and science courses. In fact, I'm pretty sure that there are many who would be happy with a "liberal arts education" that didn't include a single math or science course.
I think that there are some extremely important humanities courses that every student should take. Philosophy (logic and reasoning) is the most obvious one but there's also history and maybe even sociology. I think university students should be familiar with great literature and many other topics in the humanities programs. But I also think that every single university student needs to take (and pass) some math and science courses in order to call themselves university-educated.
This is the 21st century. Surely we can agree that science is at least as important as "liberal arts"? Maybe we should be talking about a "broad science and humanities" education as the important value that we are trying to achieve?1
I'm not sure where that leaves the thousands of students who are getting degrees in commerce and business. Perhaps we should admit that those undergraduate programs, like engineering, are not really education programs. They are job training programs.
1. I'm not talking about "astronomy for poets" and other watered-down science courses. Humanities majors should take the same courses that science majors take just as science majors take the same courses that humanities students take.
My university, the University of Toronto (Toronto, Canada), is huge. We have 60,000 undergraduates making it one of the biggest universities in North America. You'd think that undergraduate education should be a very high priority.
The university publishes an online "newspaper" called the Bulletin every Tuesday and Thursday. It's basically a PR ploy to advertise everything that's great about the University of Toronto. There was a time in the past when the Bulletin had editorials that were critical of university practice and policies but I haven't seen anything like that in years.
The latest issue has a link to an article by the President of the University, Meric Gertler. The title of the article is: Job Ready: U of T is developing new programs to help students succeed after graduation. I want to discuss two things in that article. The first is whether the university really is committed to the goals of undergraduate education (this post). The second is What does "liberal arts education" mean in the 21st century?.
I was very upset when Vincent Torley suggested that I attributed all of the evolution of chimpanzees and humans to the fixation of nearly neutral alleles by random genetic drift. He tried to convince his audience that I was rejecting natural selection as a component of that evolution. I corrected him at: Breaking news: Creationist Vincent Torley lies and moves goalposts.
When he said, "Professor Moran’s view: 22.4 million neutral mutations were what made us human," I concluded that this was so ridiculous that it had to be a deliberate misrepresentation, i.e. a lie.
Later on in the post I admitted that there was another possibility, he may just be stupid and not a liar.
He has now posted an "update" on his original post: Can the neutral theory of evolution explain what makes us human?. Here's what he says ....
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.
Intelligent Design Creationism is a huge tent that shelters all sorts of creationists ranging from Young Earth Creationists to those who could be called Theistic Evolution Creationists.1 Many of them accept common descent so they clearly don't have much of a problem with most of macroevolution.
On the other hand, there are a lot of Intelligent Design Creationists who don't accept macroevolution. It seems to me that this could only be because they are Young Earth Creationists or they believe in some other strange idea where god(s) make every species.
It's hard to figure out what they mean.
Let's look at a recent post by philosopher Vincent Torley. He didn't like my posts about macroevolution [What is "macroevolution"? ] [A chemist who doesn't understand evolution] so he decided to set me straight: Does Professor Larry Moran (or anyone else) understand macroevolution?.
The second episode of the new Cosmos series is Some of the Things That Molecules Do.
It's about evolution and it's not bad. I have four comments.
A missed opportunity. Natural selection is important and Neil deGrasse Tyson did a pretty good job of explaining it. It wouldn't have taken a big effort to mention that there's more to evolution than natural selection. He could, for example, have pointed out that some breeds of dogs are prone to certain genetic diseases or health problems because some bad mutations were accidentally fixed alone with the good ones. He could have pointed out that our eyes have a blind spot.
The Theory of Evolution is not a fact. Neil deGrasse Tyson said that the theory of evolution is a fact. This is not correct. Evolution is a fact. Evolutionary theory attempts to explain how evolution occurs. Some of the explanations, like natural selection, are facts but many aspects of modern evolutionary theory are still hotly debated in the scientific community.
We don't understand the origin of life. The episode closed with deGrasse Tyson saying the we don't understand how life began and there's nothing wrong with admitting that we don't know something. Excellent!
There are better ways of drawing DNA. I don't like the way DNA is pictured in the first two episodes, especially in the opening sequence. It looks like the bases grow out of the backbone and fuse to form base pairs. They could have drawn a more accurate representation without losing any visual appeal.
I give the episode a B+.
The winner is Philip Johnson from Switzerland.
This week's molecule (left) is actually a collection of molecules. Name all five molecules and tell me what they have in common from a biochemical perspective. Common names will do.
Email your answer to me at: Monday's Molecule #233. 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.)
Yesterday we watched two episodes of House of Cards and two of our favorite TV shows; Amazing Race and The Good Wife. We also watched a show about working on a Tudor farm and I watched the second episode of Cosmos.
According to Veronica Abbas, I wasted valuable time when I could have been reading [Recommended Reading]. She links to an article by Erin Kelley who says, Reading Books Doesn't Just Make You Literate: It Reduces Stress, Promotes Good Health, and Makes You More Empathetic. I haven't read a book in over four months and I haven't read a novel in years.
I'm doomed to be illiterate, stressed, in poor health, and the opposite of empathetic.1 It also explains why I don't volunteer to work for a non-profit organization.
1. I'm pretty sure Veronica would agree with "illiterate."
I think that universities are places where diversity of opinion should be encouraged and where fringe ideas should be protected. I'm very much opposed to letting outside interests (i.e. politicians and lawyers) decide what should and should not be taught on a university campus.
Clearly there are limits but those should be decided by faculty who understand the concept of academic freedom. It's not a good idea to offer astronomy courses on an Earth-centered solar system or geology courses based on the idea that the Earth is only 6000 years old. Those ideas are just too far out on the fringe. You're unlikely to find any university professors who want to teach such courses.
However, there are lots of other controversies that aren't so easily dismissed. If some of the more enlightened Intelligent Design Creationists want to teach a science course at my university, I would not try to prevent them. Just as I didn't try to prevent Michael Behe and Bill Dembski from speaking on my campus.
James Tour is an organic chemist. He is a Professor of Chemistry and Professor, Professor of Mechanical Engineering & Materials Science, and Professor of Computer Science at Rice University (Houston, United States). James Tour is attracting a lot of attention on the Intelligent Design Creationist websites because he is sympathetic to their main claim; namely, that evolution is wrong [see A world-famous chemist tells the truth: there’s no scientist alive today who understands macroevolution].
Tour is one of the few genuine scientists who signed the Discovery Institute’s "A Scientific Dissent from Darwinism" (2001) that stated, "We are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged." (There are very,very, few biologists who signed.)
What exactly, does Jame Tour mean? He wrote an article on his website that explains his position: Layman’s Reflections on Evolution and Creation. An Insider’s View of the Academy. I think it's interesting to discuss what he said.
He begins with ...
It's been almost a year since I commented on an Nature article by Philip Ball [see DNA: Nature Celebrates Ignorance]. Here's part of what I wrote back then ...
The main premise of the article is revealed in the short blurb under the title: "On the 60th anniversary of the double helix, we should admit that we don't fully understand how evolution works at the molecular level, suggests Philip Ball."
What nonsense! We understand a great deal about how evolution works at the molecular level.
The worst thing about the Nature article was the misuse of the Central Dogma of Molecular Biology. The second worst thing was the "revelation" that genes are regulated by regulatory sequences as if that was a new discovery. (He mentions the ENCODE results.)
I think the hardened version of the Modern Synthesis is inadequate to describe 21st century evolutionary biology. I think that it didn't adequately recognize Neutral Theory and random genetic drift and it didn't place enough emphasis on macroevolution and the possibility of hierarchical modes of evolution.
There are a whole host of scientists who want to overthrow the Modern Synthesis for a variety of other (stupid) reasons. Most of them have no idea that the Modern Synthesis has (or should have) been replaced 40 years ago.
Here's another example from last week's issue Science (March 7, 2014). Susan M. Rosenberg and Christine Queitsch have an article entitled "Combating Evolution
to Fight Disease" (Rosenberg and Queitsch, 2014). They begin with ....
The war between science and religion is fought on many fronts. One of the most remarkable campaigns is the attempt by religious zealots to discredit evolution (and science). We see this played out on creationist websites ranging from the most absurd Young Earth Creationist sites to the somewhat more subtle websites of the Intelligent Design Creationists.1
I can understand why believers want to defend their beliefs—we all do that. The part I don't get is the incredible stupidity of the main defenders of Intelligent Design Creationism and Young Earth Creationism. Not all of them, of course, but enough to make me slap my head.
Let's take Michael Egnor as an example. He is perfectly entitled to defend his Roman Catholic beliefs and to try and poke holes in evolution. But why does he have to use such stupid arguments? Why is such a person promoted on the main Intelligent Design Creationist website, Evolution News & Views (sic). Is he really the best they've got?
Let's look at his latest post: Clueless in Toronto. He begins with ....
Last December David Dobbs wrote an article entitled "Die, selfish gene die!" in which he promoted some really stupid ideas about evolution. Jerry Coyne wasted little time in showing why Dobbs was way off the mark.
Unfortunately, Dobbs didn't make the best case against the concept of the selfish gene and Jerry Coyne didn't recognize that there was a real problem.
Now the issue has resurfaced because Aeon has announced another dead horse that needs beating [Dead or Alive? Is it time to kill off the idea of the ‘Selfish Gene’? We asked four experts to respond to our most controversial essay].
Once again Jerry Coyne is up to the challenge, taking on four "experts" without breaking a sweat [The “selfish gene” redux: Aeon magazine collects opinion on the metaphor].
And, once again, everyone misses the real point.
Here's what Jerry says in his latest post.
I won’t reprise my criticisms, except to say that the metaphor of genes acting as if they are "selfish" when subject to natural selection remains perfectly good, whether or not those genes (or any bit of DNA) are part of the genome that makes proteins, regulates other genes, or comprises any bit of DNA that has the ability to get itself replicated more often than its competitors.
This is correct as far as it goes. The "selfish gene" is a reasonable metaphor if you want to think about natural selection and adaptation. It's quite reasonable to metaphorically describe genes as "selfish" in such cases.
However, I think that "selfish gene" is often used as a metaphor for all of evolution and not just for natural selection. I think that most people who read Dawkins' book take it to be about EVOLUTION and not just natural selection. They understand that Dawkins is promoting a gene-centric view of evolution—and that's okay—but they come away from reading the book by thinking that all genes are selfish.
As most of you know, I prefer to emphasize Evolution by Accident. That's not to say that natural selection (selfish genes) isn't important, it is. What I believe is that there is a lot more to evolution than just selfish genes and we should not use the selfish genes metaphor as a stand-in for all of evolution.
Once you grasp that idea, it becomes much less useful to use the term "selfish gene" as a metaphor for anything, even natural selection and adaptation. That's why I think we should stop using the term "selfish gene."
Denyse O'Leary on Uncommon Descent wonders Is “macroevolution” even a meaningful term? It’s time to ask.
Here's the problem as creationists see it ...
The evolution that Darwin’s theory accounts for (natural selection acting on random mutation) is, in the real world, small changes that don’t add up to much over the long term.
That is why the term "macroevolution" had to be invented. It was a leap of faith to assume that Darwinian "microevolution" would become "macroevolution" instead of just being washed out by other types of change (what usually really happens).
But gradually scientists are becoming less afraid to talk about this: Macroevolution apparently happens, but not by Darwinian means.
G’bye, Darwin. We packed the crumpets for ya.
Will it soon be: So long, Darwin-in-the-schools pressure groups? Gee, how they’ll be missed in the legislatures and courts.
No, wait, we’ll all be too busy figuring out what really happens in the history of life. It’s a fascinating story and now – for once – we might get to read it without all the interruptions.
I can't tell you how frustrating it is to see this kind of crap over, and over, and over. We have been trying to teach evolutionary biology to the IDiots for decades but they seem to be totally incapable of listening.
True, there was a time when biologists thought that Darwinian natural selection was all there is in evolution. They even thought that all of evolution, from changes within populations to the evolution of new phyla, could be explained solely by natural selection acting on allele frequencies within populations (Darwinism).
Most evolutionary biologists have moved on in the past half century and they now realize that macroevolution is a separate field that combines genetics, population genetics, geology, ecology and a host of other fields in order to explain the history of life. So, Denyse, it's true that macroevolution happens by means other than Darwinism even though natural selection is an important component of macroevolutionary explanations.
The only news here is that it takes IDiots so long to catch up with evolutionary biologists.
Back in the days of talk.origins, this topic (macroevolution) came up so frequently that I wrote a little essay to explain it in a way that even the most profound IDiot could understand. The latest version is from 2006: Macroevolution.
Wouldn't it be nice if the creationists could make an attempt to understand modern evolutionary theory instead of just repeating the same old tired arguments that they used 50 years ago?
The suggestion that macroevolution should be divorced from microevolution provides Creationists only with a debating point. It allows Creationists to say that there are some evolutonary theorists who distinguish the mechanisms studied in classical population genetics from those they take to be involved in large-scale evolutionary change ... But this is not to suppose that the distinction drawn by heterodox evolutionists is that favored by the Creationists.
Philip Kitcher (1982) p.150
The evolution of sexual reproduction is one of the great mysteries of biology. I've been teaching this to undergraduates for several decades but it seems that most undergraduates don't get the message. Most of them think that sex has been explained and the answer is that sexual reproduction generates diversity.
I usually give them some reviews to read and, invariably, the experts who write the reviews will say that sex is a great unsolved mystery. If the experts think that this is a mystery then why do so many people think they have the answer?
Here's what Douglas Futuyma says in the 2nd edition of Evolution (p. 340).
I am reliably informed that meetings of the Mississauga City Council1 still begin with a prayer. I'm not sure why city councilors feel the need for extra divine guidance since Mayor Hazel McCallion2 is already present in the room.
Like most places in Canada, Mississauga is a diverse community with a substantial number of nonbelievers and a substantial number of non-Christians. Prayer has no place in a secular society and beginning a City Council meeting with prayer sends out all the wrong messages. Imagine that you are a nonbeliever waiting to petition City Council over some grievance and you have to watch your council member praying before you can speak.
The evolution of recombination is part of the discussion. It's not necessarily the same as the evolution of sex but many of the explanations for the evolutionary origin of sex invoke homologous recombination.
When I asked my students to explain the evolution of sex they mostly came up with arguments about why it is advantageous to generate genetic diversity in a population. Some of this diversity requires recombination to create new combinations of alleles on the same chromosome. The problem with this argument is that for every new combination produced, an old one will be restored. As John Maynard-Smith pointed out in 1968, when genes/alleles are in linkage equilibrium then recombination does not result in a change in allele frequencies (i.e. evolution).
This led Joe Felsenstein to write the following in 1988.
It is worth noting that Maynard Smith's argument invalidates the earliest genetic argument for the evolution of recombination, that advanced by East (1918). That argument is also the one commonly found in textbooks, which tend to be a bit out of date (in this case, by over 50 years). East argued that recombination creates new genotypes. So it does. An AB/ab parent will have among its gametes not only the two types that formed it, AB and ab, but also Ab and aB if there is recombination between the two loci. But if the population is in linkage equilibrium, then somewhere else an Ab/aB parent will be undergoing recombination, which will remove Ab and aB gametes and replace them by AB and ab. These two processes will exactly cancel each other if the two types of double heterozygote, coupling (AB/ab) and repulsion (Ab/aB) are equally frequent. This will happen precisely when the population is in linkage equilibrium. In that case no new genotypes arise by recombination.
...
We have that anomalous situation that a detailed population genetic analysis analysis reveals not only that the standard explanation for the evolution of recombination will not work, but also that there is a good evolutionary reason for believing that modifiers will be selected to eliminate recombination.
Is it true that what students are being taught is wrong? What did Joe Felsenstein really mean?
Felsenstein, J. (1988) "Sex and the evolution of recombination." in The Evolution of Sex: An Examination of Current Ideas. R.E. Michod and B.R. Levin eds. 74-86. [PDF]
Last night I was at a small gathering of Liberal supporters at the Paramount restaurant on Yonge Street in Toronto. The event was organized by Omar Alghbra my former MP in Mississauga. The guest of honour was Liberal MP Marc Garneau who was Canada's first astronaut. He represents the Montreal riding of Westmount—Ville-Marie.
Marc Garneau is one of a small handful of MPs in the Federal Parliament who has a Ph.D. (Electrical Engineering, Imperial College of Science and Technology, London, England) He has always been a strong supporter of science and technology and I know that he is involved in forming science policy for the Liberals under Justin Trudeau. This was my chance to put in a good word for funding basic science so I made my pitch. I described to him how the current funding situation is hurting basic science research in the universities [Canada is destroying a generation of scientists].
It wasn't really necessary. Garneau is a strong supporter of basic science and, if elected, the Liberal Party intends to reverse the policies of the current Conservative Party under Stephen Harper. They will change the distribution of funds at NSERC and CIHR to support more curiosity motivated research and to move away from the emphasis on using science funding to support business. According to Garneau, they will also reverse the Harper decision to force NRC into short-term goal oriented technology development and return it to a broad organization that also invests in basic research.
I was impressed by the fact that Marc Garneau was just as passionate about basic research as I am. I'm confident that the Liberal Party understands the problem and will, if elected, take steps to improve the current situation. The next step is to make sure that the Harper government is booted out of office before they can do even more damage.
I think it's time we started being serious about the limitations of the RNA world as a possible explanation for the origin of life. It's simply not possible to imagine a scenario where the first catalysts are RNA molecules because that requires a primordial soups full of nucleosides and sugar molecules. It requires the spontaneous synthesis of nucleotides and their polymerization.
That ain't happening.
You can salvage the RNA world by postulating that it arose AFTER primitive metabolic pathways were established using peptide catalysts but that's the best you can do. There's a nice article in The Scientist that describes the problem [RNA World 2.0].
Here's a teaser ....
The RNA world, first posited by Francis Crick1 and others in the late 1960s, remains an attractive hypothesis. Many of the chemical hurdles that once challenged the laboratory synthesis of the molecule under presumed primordial conditions are being overcome, and in vitro evolution experiments are yielding RNA molecules that perform numerous functions, including copying themselves or other RNAs. "I don’t think there can be much doubt that RNA was a major central player as both a catalyst and an early replicator," says Nick Lane, a biochemist at the University College London whose research falls under the “metabolism first” label. "So the RNA world is absolutely correct, as far as I’m concerned, in that."
But the notion that RNA, on its own, spontaneously assembled and evolved on early Earth has fallen out of favor. More likely, whatever conditions spawned compounds as complex as nucleotides also generated other organics, perhaps early forms of modern amino acids and fatty acids, the constituent parts of proteins and membranes. "I’m not sure how many people anymore believe in a pure RNA world. I certainly don’t," says Lane. "I think the field has drifted away from that, and there’s now an acknowledgment it had to be ‘dirty.’ "
Changing Ideas About The Origin Of Life
Was the Origin of Life a Lucky Accident?
Monday's Molecule #231 [Monday's Molecule #231] was the Shine-Delgarno sequence found a few nucleotides upstream of the initiation codon in many bacterial mRNAs. It interacts (base pairs) with a sequence on the 3′ end of 16S RNA to help form the translation initiation complex. This means that bacteria can have polycistronic mRNAs (from operons) and internal translation initiation. The winners were Keith Conover and Nevraj Kejiou. That's two weeks in a row that an undergraduate from the University of Toronto has won. I will be taking them to lunch. I encourage undergraduates from far, far away to hurry up and send in an answer to this week's molecule!
This week's molecule (left) is covalently bound to the lysine side chain of a protein. It exists in two distinct configurations that can be interconverted by a well-known chemical reaction. Name the two different configurations (common names only) and explain the significance of the reaction.
Email your answer to me at: Monday's Molecule #232. 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.)
Saturday night was the night when most people in North American turned their clocks forward one hour for "Daylight Saving Time."1 TV, radios, and newspapers are whining about the fact that everyone was going to lose an hour's sleep. Some of the comments on my radio station advise people to avoid driving today (Monday) because you might be suffering from sleep deprivation.
This all seems very strange to me. Is it true that most people are so unfamiliar with traveling across time zones that turning your clock back one hour is a really big deal?
And what's this about losing one hour's sleep? When I got out of bed on Sunday morning it was about one hour later (on the clock) than the time I usually wake up on Sunday morning. I didn't lose an hour's sleep. The only people who lost an hour's sleep on Saturday night are those who wake up every Sunday morning to an alarm clock. Are you one of those people?
It's a little bit different on Monday morning when, I imagine, most people have to wake up to an alarm clock in order to get to work. I'm not one of those people. However, even on Sunday night the only way you lose an hour's sleep is if you went to bed an hour later than normal.
Somewhere along the way I have lost an hour of my day but it's not going to come out of sleep time. That would be silly. If I ever feel sleep deprived I'll just go to bed earlier.
How about the rest of you? Do you really give up an hour of sleep in the days following the shift to Daylight Savings Time?
More accurately known as "Daylight Shifting Time."
Later on today I'm giving a talk at Western University (London, Ontario, Canada)1 The subject is blogging.
I realized while preparing my talk that there were lots of things I didn't know for sure so here are some questions that you may be able to help with.
Most popular biology blogs
I don't know for sure which biology blogs are the most popular. I'm pretty sure that Pharyngula is still on top with respect to the number of views per day and I'm pretty sure that Why Evolution Is True is in the top ten but what about others? Do any of you know?
Best biology blogs
The best blogs aren't necessarily the most popular. I have my own opinion about the best blogs but my fear is that I've missed some blogs that I should be reading. What do you think? What are the best biology blogs?
Why do you read and comment?
I've talked to a lot of bloggers so I'm pretty sure I have a good idea about why we write blogs. But I realized that I was much less sure about why people read blogs and why people comment on blogs. What do you get out of reading blogs and why do you post comments? Do you think all scientists and science students should read the science blogs? (I don't.)
Have blogs changed anything?
Have blogs had much of an impact on science? I can think of a few examples such as the Arsenic Affair and the ENCODE Publicity Hype Fiasco where bloggers had an impact but I'm not sure these are significant in the log run. Is blogging just another kind of social interaction that really doesn't change the way science is done?
1. Formerly the University of Western Ontario. The talk is in the North Campus Building room 114 at 11:30 am.
THEME:
Transcription
The Journal of Biological Chemistry (JBC) publishes a little booklet of the "best of jbc." The latest copy arrived in the mail a few days ago and it alerted me to a paper published one year ago on the structure of Escherichia coli RNA polymerase σ70 holoenzyme (Murikami, 2013).1
The control of transcription initiation is a very important topic in biochemistry and molecular biology and the events in E. coli are the model for transcription initiation in all other species. We know more about RNA polymerase and promoter sites in E. coli than in any other species.
