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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.
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.
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.
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.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.
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.
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.
New Scientist: The Accommodationist Issue
I subscribe to New Scientist. Many years ago, I decided that it was the best of the popular science magazines—better than Scientific American, National Geographic, SEED (now defunct), and Discover. Recently, however, I been having second thoughts as the quality of the articles deteriorates and more and more pseudoscience and wrong science is making its way into the magazine. The issue of March 17-23, 2011—The God Issue—is the last straw. This is no longer a science magazine.
It's not because the topic is out-of-bounds. Quite the contrary, I think it's perfectly appropriate to address the conflict between science and religion. There's even a good article in there; it's the one by Victor Stenger. Stenger argues convincingly that science conflicts with the existence of all personal gods. It's possibly compatible with a strictly deist god but nobody believes in such a god.
The problem is with all the other articles which are accommodationist to various degrees. Several of them flatly contradict science (and common sense). One of them (by Alain de Botton) advocates that atheists adopt some of the practices of religion as if religion has a monopoly on being nice.
You only have to read the editorial to see how bad things have become ....
"GIVE me the child until he is seven, and I will show you the man." This Jesuit maxim epitomises how many of us perceive religion: as something that must be imprinted on young minds.The editors seem to have been completely bamboozled by the article entitled Born Believers. The author is Justin L. Barrett of Fullier Theologial Seminary in Pasadena, California (USA). Barrett argues ....
The new science of religion begs to differ. Children are born primed to see god at work all around them and don't need to be indoctrinated to believe in him (see "The God issue: We are all born believers").
This is just one of many recent findings that are challenging standard critiques of religious belief. As we learn more about religion's biological roots, it is becoming clear that secularists are often tilting at windmills and need to rethink.
Another such finding is that belief in a god or gods does appear to encourage people to be nice to one another. Humans clearly don't need religion to be moral, but it helps (see "The God issue: Religion is the key to civilisation").
An interesting corollary of this is a deeply held mistrust of atheists (see "In atheists we distrust"). In fact, atheists might consider themselves as unrecognised victims of discrimination. In a recent opinion poll, Americans identified atheists as the group they would most disapprove of their children marrying and the one least likely to share their own vision of American society. Self-declared atheists are now the only sizeable minority group considered unelectable as president.
Such antipathy poses a dilemma for opponents of religion, and may explain why "militant atheism" has failed to make headway.
Secularists would also do well to recognise the distinction between the "popular religion" that comes easily to people's minds and the convoluted intellectual gymnastics that is theology. Attacking the latter is easy but will do little to undermine religion's grip (see "The God issue: Science won't loosen religion's grip").
This is not an apologia for god. Religious claims still wither under rational scrutiny and deserve no special place in public life. But it is a call for those who aspire to a secular society to approach it rationally - which means making more effort to understand what they are dealing with. Religion is deeply etched in human nature and cannot be dismissed as a product of ignorance, indoctrination or stupidity. Until secularists recognise that, they are fighting a losing battle.
Drawing upon research in developmental psychology, cognitive anthropology and particularly the cognitive science of religion, I argue that religion comes nearly as naturally to us as language. The vast majority of humans are "born believers", naturally inclined to find religious claims and explanations attractive and easily acquired, and to attain fluency in using them. This attraction to religion is an evolutionary by-product of our ordinary cognitive equipment, and while it tells us nothing about the truth or otherwise of religious claims it does help us see religion in an interesting new light.Barrett quotes a few studies in support of his claim but those studies don't really say what he thinks they say. It makes no sense to say that young children find religious claims and expectations attractive unless they have heard these explanations from adults.
I don't remember a time in my childhood when I spontaneously created a supernatural being who expected me to behave in certain ways. I never saw any evidence that my children needed to create gods and I don't see any evidence that my two-year-old granddaughter needs to imagine sky daddies in order to understand the world around her.
There are millions of children in Europe who are growing up as second and third generation atheists and I can't imagine that their parents are upset because the children are turning out to be "born believers." The idea is ridiculous. It could only come from a culture where young children are being constantly brainwashed by stories about gods. There's no such thing as an innate attraction to religion in a culture with no religion in the first place.
Oh, and one other thing, it's not true that belief in one of the gods makes you a nicer person. If that were true then America would be one of the kindest, nicest, societies among all Western industrialized nations. And Saudi Arabia would take the prize for the nicest society in the world. And you sure as hell wouldn't want to live in evil, crime-ridden Sweden or Holland.
Richard Dawkins Defends the Reason Rally
Richard Dawkins writes in yesterday's Washington Post [Who would rally against reason?].
March 24th is a landmark date for Washington, D.C. Thousands will converge on the world’s leading capital city to celebrate the crowning human virtue of reason.I agree with Dawkins. "Reason" and rationality is what we should be promoting. If we are successful, then religion will disappear and atheism will be the default position. As Dawkins puts it in The God Delusion, the real battle is between rationalism and superstition or between reason and superstition.
How have we come to the point where reason needs a rally to defend it? To base your life on reason means to base it on evidence and logic. Evidence is the only way we know to discover what’s true about the real world. Logic is how we deduce the consequences that follow from evidence. Who could be against either? Alas, plenty of people, which is why we need the Reason Rally.
Dawkins has a series of videos called The Enemies of Reason. They are promoted as: "Professor Richard Dawkins confronts the epidemic of irrational, superstitious thinking with logic, observation and evidence - in other words, through reason." Here's the episode on superstitious beliefs in health and medicine.
It's obvious that anyone who opposes vaccination and/or promotes alternative medicine is an enemy of reason. It's difficult to imagine how such a person could be invited to speak at the Reason Rally in Washington, right?
So why are Senator Tom Harkin and Bill Maher speaking if they are clearly enemies of reason [The Reason Rally ought to have some standards]?
It's because some of the organizers of the Reason Rally do not agree with Richard Dawkins. They see this event as an atheist rally and the speakers are being invited because they are prominent atheists, not necessarily rationalists. Hemant Mehta of Friendly Atheist is one of those people [Plan Your Own Reason Rally and Then Tell Me How It Goes].
Look, the organizers spent a long time listening to the suggestions of dozens of people (representing tens of thousands of atheists) regarding who should speak at the Rally. They did everything in their power to contact all the “big names” that people said they wanted to hear at the Rally. They rustled up and managed the hundreds of thousands of dollars in funding needed to put on an event of this magnitude. They got every major organization in our movement to work together to make this work — and that’s not an easy thing to do. They had to deal with the speakers complaining about their prominence on our website (yep, it happened).This is going to be confusing. Who's right? Is this a Reason Rally as Dawkins and PZ Myers think or is it an Atheist Rally as Hemant believes?
Just about everyone believes in something irrational. Including atheists. So, yes, you’re going to hear people at the Rally who hold ideas we think are completely unreasonable. Maybe even harmful.
If we got rid of every speaker who held an irrational belief, there would be no one left on that stage.
So deal with it.
I’m not saying you shouldn’t call them out where they’re wrong. Have at it. I did it, too. In many cases, they deserve it. But to suggest the organizers are at fault for inviting really famous atheists who hold some view you don’t agree with is absurd. Almost as ridiculous as faulting them for accepting a greeting from a sitting U.S. senator who stands to lose a lot more than he’ll gain for addressing our crowd.
Monday, March 19, 2012
I Rank Number One on Google
I was searching through some old posts today and I came across I Rank Number One on Google from October 2007. The idea was to come up with five words or phrases where Google would return something by you at the top of the page.
Back then I picked ...
- Larry Moran
- Sandwalk
- Three Domain Hypothesis
- adaptationist-pluralist
- is there a genetic component to intelligence
- Larry Moran
- Sandwalk
- Three Domain Hypothesis
- adaptationist-pluralist
- random genetic drift
I'm giving a lecture tomorrow on the Three Domain Hypothesis and why it is no longer valid. I still have the top three hits for this topic on Google. In case you've forgotten, you can read about it at: Theme: The Three Domain Hypothesis.
1. "Paul Zachary Myers" works, but that's cheating.
Labels:
Blogs
Dynamics and Sloppiness in Protein Synthesis
Protein synthesis can be divided into three stages.
First, there's the initiation stage when a ribosome binds to the initiation codon in messenger RNA (mRNA) and the translation initiation complex forms by recruiting additional components.
Second, there's the elongation stage when the elongation complex moves along the mRNA translating the coding region and producing a polypeptide chain. The elongation rate is relatively constant but from time to time the elongation complex pauses at particular sites that are difficult to translate.
Finally, the elongation complex encounters a termination site where it disassembles and the ribosome with its various factors is released from the mRNA.
We Are All Apes
Richard Dawkins created a bit of a stir among the theists by claiming that he is an African ape.
Someone named Vasko Kohlmayer was partularly upset so he wrote up a "rebuttal" for the Moonie newspaper The Washington Times: Is Richard Dawkins an Ape?.
I don't much care about the opinions of theists like Vasko Kohlmayer because they have an obvious agenda. Scientific arguments are meaningless to them.
But I do care about the opinions of other scientists and philosophers. Jerry Coyne explains why we are apes and why it's not a good idea to say that people living in Oxford or Chicago are African apes [Washington Times denies that Richard Dawkins is an ape]. I agree with Jerry.
John Hawks disagrees [Humans aren't monkeys. We aren't apes, either.]. He claims that the term "ape" is not a legitimate phylogenetic term and therefore is doesn't have to refer to a monophyletic group.
Chimpanzees are apes. Gorillas are apes, as are bonobos, orangutans, and gibbons. We routinely differentiate the "great apes" from the "lesser apes", where the latter are gibbons and siamangs. Humans are not apes. Humans are hominoids, and all hominoids are anthropoids. So are Old World monkeys like baboons and New World monkeys like marmosets. All of us anthropoids. But humans aren't monkeys.I don't agree with this distinction. There's nothing to be gained by saying that our closest relatives are apes but we aren't.
John Wilkins thinks we are apes [Are humans, apes, monkeys, primates, or hominoids?]. John argues like a philosopher but, in this case, he's right.
It is not possible to stem the tide of linguistic change, as the Académie Française has found out repeatedly. If experts can redefine terms influentially, then there is nothing wrong with that so long as it doesn’t confuse the experts. Using paraphyletic terms (that is, group names that denote what is left of the group once a subset has been removed) is a Very Bad Idea that hangs on in science, but it need not hang on in folk usage. And there’s nothing wrong with saying “humans are apes”, because, on the best construal of what those terms denote, they are.
Neil Shubin’s excellent book Your Inner Fish makes a similar point. Where once a “fish” was anything that lived in water (including swans, geese, alligators and crocodiles, whales, and water snakes), it came to mean a vertebrate that had gills and fins and scales. Shubin shows how the Gnathostomes (jawed fishes) includes land vertebrates, including mammals and ultimately us, as well. Language can change…
UPDATE: Brian Switek of Laepaps weighs in with: I’m an Ape, and I’m Also a Fish.
Monday's Molecule #162
The last few challenges have been too easy so I'm going to make this week's molecule a bit more difficult. Not only do you have to identify the molecule but you also have to identify each of the four residues that are sugar derivatives. What is the molecule in blue and what are the other three sugary-looking residues?
Be sure to give a complete unambiguous name—that means getting the stereochemistry correct.
Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post correct answers to avoid embarrassment. The winner will be treated to a free lunch. I'll be setting up a lunch for this Thursday so expect an email message. If I owe you a lunch, it wouldn't hurt to remind me in case I forget you.
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.
UPDATE: The molecule is ganglioside GM2. The residues are N-acetyl-α-neuraminic acid (blue), N-acetyl-β-D-galactosamide, β-D-galactose, and β-D-glucose (left to right). You were asked to be specific in naming the sugar residues. Several people got the molecule correct but nobody named the sugar residues in a completely unambiguous manner, although the correct names are implied in the formal name of the molecule. There is no winner 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
Sunday, March 18, 2012
The "Reason Rally" Will Have Everything But Reason.
A lot of people are going to Washington next Saturday to stand1 near the reflecting pool for eight hours listening to short speeches and videos during the Reason Rally.
One of the speakers will be PZ Myers and he is rightly upset about some of the other speakers who don't exactly fit the criterion of "reason." Read what he has to say about Senator Tom Harkin and Bill Maher [The Reason Rally ought to have some standards].
Was Deepak Chopra busy on 24 March? Did Oprah have a hair appointment? Maybe it’s not too late to sign up John Edward — he could channel Ingersoll and Russell and Sagan for us, although of course we’d have to be content with him guessing at their words one letter at a time.So what's the point of having a "Reason Rally" if you schedule talks from known kooks who oppose reason?
I suspect that a lot of people will be wandering off to look at the cherry blossoms behind the Jefferson Memorial. I hope the size of the crowd isn't an embarrassment.
You can buy a ticket for the seating area in front of the stage if you're willing to pay $500, $1000, or $5000 [VIP Seating].
Friday, March 16, 2012
John Mattick Wins Chen Award for Distinguished Academic Achievement in Human Genetic and Genomic Research
Shame on the Human Genome Organization (HUGO). It has awarded a prestigious prize (US $10,000) to John Mattick, director of the Centre for Molecular Biology and Biotechnology at the University of Queensland in Brisbane, Australia. Here's the report from the Sydney Morning Herald.
Making something of junk earns geneticist top award
WHEN Sydney geneticist John Mattick suggested junk DNA was anything but rubbish he was challenging an assumption that had underpinned genetics for 50 years.
''The ideas I put forward 10 years ago were quite radical but I thought I was right,'' Professor Mattick said.
He was. And tomorrow he will become the first Australian honoured with the Chen Award for distinguished academic achievement in human genetic and genomic research, awarded by the Human Genome Organisation.
For decades after James Watson and Francis Crick discovered DNA was a double helix, scientists believed most genes were the written instructions for proteins, the building blocks of all body processes. The assumption was true for bacteria but not complex organisms like humans, said Professor Mattick, the new executive director of the Garvan Institute.
In humans, more than 95 per cent of the genome contains billions of letters that do not make proteins, called non-coding DNA. ''When people bumped into all this DNA that didn't make proteins they thought it must be junk,'' he said. But Professor Mattick felt it was unlikely that useless material would survive hundreds of millions of years of evolution.
He found that the non-protein-coding sections of DNA had a function, to produce RNA.
"The obvious and very exciting possibility was that there is another layer of information being expressed by the genome - that the non-coding RNAs form a massive and previously unrecognised regulatory network that controls human development.''
Many scientists now believe this RNA is the basis of the brain's plasticity and learning, and may hold the secret to understanding many complex diseases.
Thursday, March 15, 2012
Happy Ides!
Today is the Ides of March a famous day in European history because of Brutus, Cassius and a bunch of other Roman dudes.
Did you ever wonder what an "ide" was. Here's the explanation from Wikipedia [Ides of March].
The word Ides comes from the Latin word "Idus" and means "half division" especially in relation to a month. It is a word that was used widely in the Roman calendar indicating the approximate day that was the middle of the month. The term was used for the 15th day of the months of March, May, July, and October, and the 13th day of the other months.I think you have to be more than 50 years old to appreciate this skit. You might have to be Canadian.1
1. Wayne & Shuster are graduates of the University of Toronto.
Labels:
History
What Does a Eukaryotic Ribosome Look Like?
There's a picture of a yeast (Saccharomyces cerevisiae) ribosome on the cover of the Dec. 16, 2011 issue of Science. The paper inside by Ben-Sham et al. (2011) describes the structure at 3Å resolution.
There's nothing revolutionary here but I thought I would show you the structure just to emphasize a particular point. You can see the same image below without the distracting orange background.
Most of the ribosome is composed of RNA (silver-gray strands). You can see that a lot of this single-stranded RNA forms short double-helical regions when the RNA folds back on itself. Small ribosomal proteins (various colors) decorate the surface of the ribosome by binding to specific regions of the ribosomal RNA.
The overall impression is that the ribosome is a big ball of RNA with a small amount of protein. The actual site of translation, where messenger RNA is translated into a polypeptide, takes place in the middle of the ribosome near the hole you see in this structure. Translation is catalzyed by the RNA component of the ribosome, not by the ribosomal proteins.
I don't know about the rest of you but I grew up with an electron-micrographic image of a ribosome in my head and I just assumed that what I was seeing was a large glob of protein. If course I realized that there was a huge amount or RNA in there somewhere but I didn't think it contributed very much to the dark blobs in the cell.
When the first crystal structures of ribosomes were published I had to stare at them for quite some time in order to purge the old images from my mind and adopt a new perspective.
Eukaryotes have 79 ribosomal proteins and prokaryotic ribosomes have only 52 proteins. There are prokaryotic ribosomal proteins that have no homoogues in eukaryotes and 33 of the eukaryotic ribosomal proteins have no homologues in bacteria—they are eukaryotic specific. Furthermore, many of the eukaryotic proteins differ considerably from their bacterial homologues. (Mostly by extensions of the poly peptide chain.)
The protein components of ribosomes are not highly conserved. One gets the impression that they don't contribute much to the function of a ribosome—an impression confirmed by the fact that the RNA by itself can catalyze polypeptide synthesis. They may help stabilize the three-dimensional structure of the ribosome.
[Image credit: The bottom image is "courtesy of Prof Marat Yusupov (IGBMC, Strasbourg)" from The 9th international Conference on Ribosome Synthesis that takes place this summer in Banff, Alberta, Canada.]
Ben-Shem A, Garreau de Loubresse N, Melnikov S, Jenner L, Yusupova G, Yusupov M. (2011) The structure of the eukaryotic ribosome at 3.0 Å resolution. Science 334:1524-1529. (Epub 2011 Nov 17). [doi: 10.1126/science.1212642]
Monday, March 12, 2012
Monday's Molecule #161
Some species make this molecule for a very special reason. Identify the molecule using the common name and the IUPAC name. You must also say why it's important for some species.
Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post correct answers to avoid embarrassment. The winner will be treated to a free lunch with a famous Nobel Laureate, or with me if the Nobel Laureate isn't available.
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.
UPDATE: The molecule is taurocholate (2-{[(3α,5β,7α,12α)-3,7,12-trihydroxy-24-oxocholan-24-yl]amino}ethanesulfonate). Taurocholate is a bile salt in mammals. This week's winners are Bill Chaney and Raul A. Félix de Sousa.
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
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