The pathway of information flow runs from DNA to RNA to proteins. There are a bunch of fundamentally important steps in this pathway including transcription, RNA processing, and translation.
Translation, or protein synthesis, is the process that utilizes the information in Messenger RNA (mRNA) to build a polypeptide (protein). Over the past few decades this process has been worked out in hundreds of labs all around the world but recent progress has been quite remarkable.
One of the key players in translation is the ribosome. (The others are mRNA, tRNAs and translation factors.) The ribosome and the other translation components form a complex molecular machine. The ribosome itself is complex, consisting of several RNA molecules (ribosomal RNAs) and several dozen proteins.
Thanks to the work of Harry Noller, we now know that one of these ribosomal RNAs is the molecule that actually catalyzes the formation of a peptide bond. The basic activity in proteins synthesis doesn't require a protein enzyme, it's an RNA molecule that does the job.
Thanks to this year's Nobel Laureates, and Harry Noller, we now know the structure of the ribosome at the molecular level and we know where the tRNAs and the translation factors bind.
We've known about these sites—the P and A sites are the most important—for some time but now we have a real picture of what they look like in the actual molecule. And it's led to some significant advances in our understanding of this important biological process.
This is basic science. It's not some speculative discovery that may or may not be a breakthrough and may or may not cure cancer (probably not). This is the stuff that goes into the textbooks. This is what science is all about.
The 2009 Nobel Prizes provide science writers with an excellent opportunity to highlight some discoveries that are really important in biology. You'd think that science writers would be all over this.
Where are they when the work is worth writing about? Are they going to be as silent about this as they were about the Nobel Prize for transcription in 2006?
A few weeks ago I blogged about an important series of papers on the evolution of the glucocorticoid receptor gene [see You Can't Go Home Again]. This is work from the Thornton lab and it shows the effect of accumulating neutral mutations over millions of years. I like the papers because it demonstrates clearly where Michael Behe goes wrong in his latest book The Edge of Evolution.
Not surprisingly, Michael Behe read the papers. Surprisingly, he actually thought they helped his case rather that hurt it [see Nature Publishes Paper on the Edge of Evolution]. I was going to follow up on this since it was the reason I brought the papers to your attention in the first place. Now I'm glad I didn't because Carl Zimmer has done a much better job.
This is a really important article for a variety of reasons. You must read it if you want to learn about modern concepts in evolution.
Here's an excerpt from Thornton's letter that should induce you to visit the rest of the article.
Thanks for asking for my reaction to Behe’s post on our recent paper in Nature. His interpretation of our work is incorrect. He confuses “contingent” or “unlikely” with “impossible.” He ignores the key role of genetic drift in evolution. And he erroneously concludes that because the probability is low that some specific biological form will evolve, it must be impossible for ANY form to evolve.
Behe contends that our findings support his argument that adaptations requiring more than one mutation cannot evolve by Darwinian processes. The many errors in Behe’s Edge of Evolution — the book in which he makes this argument — have been discussed in numerous publications.
In his posts about our paper, Behe’s first error is to ignore the fact that adaptive combinations of mutations can and do evolve by pathways involving neutral intermediates. Behe says that if it takes more than one mutation to produce even a crude version of the new protein function, then selection cannot drive acquisition of the adaptive combination.
Here's how my family descends from Charlemagne. The last people on the list are my maternal grandparents. I think the data is accurate but I look forward to any corrections or comments.
UPDATE: I'm almost certainly NOT related to Charlemagne in the lineage shown below. Link #34 is wrong. The father of Ruhama Hill is NOT William Hill of Fairfield, Connecticut but Captain John Hill of Westerley, Rhode Island.
UPDATE (Jan. 2015): An informed read has pointed out that Julianne FiztMaurice (#18) is the daughter of Maurice FitzMaurice and his first wife, Matilda de Predergast, and not his second wife Emmiline de Longspree (#17) as I've shown.
Thousands of amateur genealogists have contributed to a huge database of family relationships, including genetic analyses. What does this teach us about human populations and evolution?
It may seem like a ridiculous question to ask whether you are a descendant of Charlemagne, who was crowned Emperor on December 25, 800. If you live in Asia or Africa, or your ancestors are from Asia or Africa, then you are probably not a descendant of Charlemagne.
But if any of your ancestors lived in Europe, especially western Europe, then it's almost certain that Charlemagne is one of your ancestors. No matter where your ancestors are from they probably share a common ancestor with everyone else from that region. What's surprising is that many of those common ancestors lived only 1200 years ago.
I'm talking about big regions here, like most of Europe or Asia, or Africa. There's a remarkable amount of inbreeding among human populations at that scale. It's a good example of how evolution works. It's populations that evolve.
Remember that it's populations that evolve, not individuals. With only a few exceptions, species are subdivided into numerous populations with restricted gene flow between them. The sub divisions range from very large group called races, or subspecies, to progressively smaller populations down to local demes or extended families. In small populations, alleles can become rapidly fixed by random genetic drift but the existence of these populations means that it is much more difficult for these alleles to spread to the rest of the species. What we expect to see under those conditions is races or demes that differ substantially in their allele frequencies.
The explosion in amateur genealogy in recent years has highlighted these kinds of population structures in our own species. More and more people are putting their genealogical research on publicly accessible databases such as ancestry.com and many others. The collective result of these, mostly amateur, investigations is remarkable. It means that every one of us can make a family tree.
Well, perhaps not everyone. There's a huge bias towards Caucasians in the genealogy databases. There are many reasons for this bias but we won't go into them in this post. The important result is that we can all learn something about human populations from this data even if it doesn't include your own ancestors.
The other recent development is the increasing number of people who are having their DNA analyzed and posting the results online. This is much more important since people all over the world are participating and we will soon have a good picture of the genetic structure of today's populations. This complements the family tree data in the same way that gene phylogenies complement the fossil record.
What about Charlemagne? Amateur European genealogists have to do a lot of work to document their ancestors back four or five generations. This takes them to the 1800s (30 years per generation).1 At that point in time they have 16 or 32 direct ancestors and chances are they'll be able to hook up with others who share these ancestors. The farther back you go on your own, the greater the chances that someone will have researched your ancestor.
The idea that many of us are related to Charlemagne is not new. Here's what they say on the Genealogy of Presidents website.
Genealogists have mathematically demonstrated how all Americans of European descent must be related to Charlemagne. In this regard, genealogists have established the exact lines of descent from Charlemagne for 14 U.S. Presidents. Two of these are President George W. Bush and his father President George H.W. Bush. Other Presidents whose descent from Charlemagne have been traced include: George Washington, Ulysses Grant, Franklin Roosevelt, Teddy Roosevelt, and Gerald Ford. To demonstrate how we are all related, the New England Historical Society has researched the genealogy of Barack Obama and determined that on his mother's side he is related to six other previous presidents: George W. Bush, George H. W. Bush, Lyndon Johnson, Harry Truman, Gerald Ford, and James Madison. Presumably, if Barack Obama's ancestry on his mother's side could be traced far enough back, he also would be shown to be descended from Charlemagne. Meanwhile, on his father's side, we are all related to President Barack Obama since anthropologists have determined that all modern humans are descended from a common African ancestor.
If you examine the List of United States Presidents by genealogical relationship you'll see that 19 US Presidents are descendants of British royalty and therefore, almost certainly, descendants of Charlemagne. Note that US Presidents are not royalty, they are, to all intents and purposes, ordinary citizens, just like you and me.
It's almost trivial to find connections to the US Presidents if you have ancestors who settled in the British colonies in the 1600s. I'm related to George Bush, for example, through the Shermans of Rhode Island and Connecticut. The good news is that I'm also related to Winston Churchill though the same family.
The amazing thing about genealogy is how closely related everyone is once you start looking. This isn't so amazing to population geneticists.
It's not so hard for North Americans to find European ancestors but many lineages terminate because parish records have not been preserved and because there are no other sources for the ancestors of average citizens. But every now and then you'll stumble upon lineages that have been well researched. Among my own ancestors for example there are half a dozen lineages that reach back to the 1400s and beyond. All I did was find the connections to those lineages.
The history of European nobility is well known. Chances are, you have at least one ancestor who connects to the various Dukes, barons, Counts, and Knights and their spouses in medieval times . A large percentage of the nobility of the European nobility can claim descent from Charlemagne. He had 20 children.
With a little effort, almost everyone of European descent can find the path to Charlemagne. If your ancestors are from England or Scotland your connection often runs through William of Normandy and a bunch of other tourists from France who visited England in 1066. Be careful, though, because there are many incorrect genealogies on the web and you'll need to do some fact checking. I found three different connections to nobility but two of them were figments of someone's overactive imagination. [See My Family and Other Emperors for my relationship to Charelmeange.]
Expert genealogists, as opposed to amateurs, are very frustrated by these errors on the internet. Because of the nature of the databases, it's very hard to remove errors once they start being incorporated into various genealogies.
The fact that all Europeans have several recent common ancestors tells us a lot about the genetic makeup of this population. It is quite homogeneous and there's a lot of inbreeding. It seems to be extremely rare to discover a non-European ancestor once one goes back a few hundred years. (It's much more common in recent times.) I presume this lack of outbreeding also applies to Asians, Africans, and all other groups.
Given that the average generation is 30 years2, if you go back to 800 that's about 40 generations. Potentially you have 240 ancestors. That's more than 1 trillion ancestors alive in 800. I don't know what the population of Europe was in 800 but I strongly suspect it wasn't even close to one trillion people. I suspect it was only about 25 million. It's not surprising that you are related to many of them.
It would be interesting to know how many people who were alive in 800 have direct descendants who are alive today. Maybe there's a way of calculating this?
1. In my case it was my mother who did/does all the work. I just surfed the internet using her data.
2. The actual calculated value for my ancestors is 29 years per generation.
"for their discoveries concerning the function of single ion channels in cells"
Erwin Neher (1944 - ) and Bert Sakmann (1942 - ) won the Nobel Prize for developing a technique to measure the voltage changes produced by single ion channels in cell membranes.
This is a remarkable achievement. The ion channel is in it's natural environment and the voltage change it produces is minuscule. The technique, called the "patch clamp", could not have been discovered without sensitive instruments developed in other disciplines.
1991 is part of the modern era on the Nobel Prize website so there's an excellent press release available to explain the award and describe the science. Here's the Press Release. THEME: Nobel Laureates
Summary
Each living cell is surrounded by a membrane which separates the world within the cell from its exterior. In this membrane there are channels, through which the cell communicates with its surroundings. These channels consist of single molecules or complexes of molecules and have the ability to allow passage of charged atoms, that is ions. The regulation of ion channels influences the life of the cell and its functions under normal and pathological conditions. The Nobel Prize in Physiology or Medicine for 1991 is awarded for the discoveries of the function of ion channels. The two German cell physiologists Erwin Neher and Bert Sakmann have together developed a technique that allows the registration of the incredibly small electrical currents (amounting to a picoampere - 10-12A) that passes through a single ion channel. The technique is unique in that it records how a single channel molecule alters its shape and in that way controls the flow of current within a time frame of a few millionths of a second.
Neher and Sakmann conclusively established with their technique that ion channels do exist and how they function. They have demonstrated what happens during the opening or closure of an ion channel with a diameter corresponding to that of a single sodium or chloride ion. Several ion channels are regulated by a receptor localized to one part of the channel molecule which upon activation alters its shape. Neher and Sakmann have shown which parts of the molecule that constitute the "sensor" and the interior wall of the channel. They also showed how the channel regulates the passage of positively or negatively charged ions. This new knowledge and this new analytical tool has during the past ten years revolutionized modern biology, facilitated research, and contributed to the understanding of the cellular mechanisms underlying several diseases, including diabetes and cystic fibrosis.
What Happens Inside the Cell?
Inside the cell membrane there is a well-defined environment, in which many complex biochemical processes take place. The interior of the cell differs in important respects from its outside. For example the contents of positive sodium and potassium ions and negatively charged chloride ions are quite different. This leads to a difference in electrical potential over the cell membrane, amounting to 0.03 to 0.1 volts. This is usually referred to as the membrane potential.
The cell uses the membrane potential in several ways. By rapidly opening channels for sodium ions the membrane potential is altered radically within a thousandth of a second. Cells in the nervous system communicate with each other by means of such electrical signals of around a tenth of a volt that rapidly travel along the nerve processes. When they reach the point of contact between two cells - the synapse - they induce the release of a transmitter substance. This substance affects receptors on the target cell, often by opening ion channels. The membrane potential is hereby altered so that the cell is stimulated or inhibited. The nervous system consists of a series of networks each comprised of nerve cells connected by synapses with different functions. New memory traces in the brain are for example created by altering the number of available ion channels in the synapses of a given network.
All cells function in a similar way. In fact, life itself begins with a change in membrane potential. As the sperm merges with the egg cell at the instant of fertilization ion channels are activated. The resultant change in membrane potential prevents the access of other sperm cells. All cells - for instance nerve cells, gland cells, and blood cells - have a characteristic set of ion channels that enable them to carry out their specific functions. The ion channels consist of single molecules or complexes of molecules, that forms the wall of the channel - or pore - that traverses the cell membrane and connects the exterior to the interior of the cell (Figure 1B and 1D). The diameter of the pore is so small that it corresponds to that of a single ion (0.5-0.6 millionths of a millimetre). An immediate change in the shape of the molecule leads to either an opening or a closure of the ion channel. This can occur upon activation of the receptor part of the molecule (Figure 1D) by a specific signal molecule. Alternatively a specific part of the molecule that senses changes in membrane potential can open or close the ion channel.
Figure 1. Registration of the flow of current through single ion channels using the recording technique of Neher and Sakmann. A schematically shows how a glass micropipette is brought in contact with the cell, and B, using a higher magnification, a part of the cell membrane, with ion channels, in close contact with the tip of the pipette. The interior of the pipette is connected to an electronic amplifier. C shows a channel in greater magnification with its receptor facing the exterior of the cell and its ion filter. D shows the current passing through the ion channel as it opens.
Neher and Sakmann Record the Electric Current Flowing Through a Single Ion Channel
It has long been known that there is a rapid ion exchange over the cell membrane, but Neher and Sakmann were the first to show that specific ion channels actually exist. To elucidate how an ion channel operates it is necessary to be able to record how the channel opens and closes. This appeared elusive since the ionic current through a single ion channel is extraordinarily small. In addition, the small ion channel molecules are embedded in the cell membrane. Neher and Sakmann succeeded in solving these difficulties. They developed a thin glass micropipette (a thousandths of a millimeter in diameter) as a recording electrode. When it is brought in contact with the cell membrane, it will form a tight seal with the periphery of the pipette orifice (Figure 1A, B). As a consequence the exchange of ions between the inside of the pipette and the outside can only occur through the ion channel in the membrane fragment (Figure 1B). When a single ion channel opens, ions will move through the channel as an electric current, since they are charged. Through a refinement of the electronic equipment and the experimental conditions they succeeded in measuring this "microscopical" current by laborious methodological developments during the seventies (Figure 1C).
How Does an Ion Channel Operate?
Ion channels are of different types. Some only permit the flow of positively charged sodium, potassium or calcium ions, others only negatively charged chloride ions. Neher and Sakmann discovered how this specificity is accomplished. One reason is the diameter of the ion channel, which is adapted to the diameter of a particular ion. In one class of ion channels, there are also two rings of positively or negatively charged amino acids. They form an ionic filter (see Figure 1D), which only permits ions with an opposite charge to pass through the filter. In particular Sakmann through a creative interaction with different molecular biologists elucidated how the different parts of the ion channel molecule(s) operate. Neher and Sakmann's scientific achievements have radically changed our views on the function of the cell and the contents of text books of cell biology. Their methods are now used by thousands of scientists all over the world.
The Study of Secretory Processes
Nerve cells, as well as hormone-producing cells and cells engaged in the host defence (like mast cells) secrete different agents. They are stored in vesicles enclosed by a membrane. When the cell is stimulated the vesicles move to the cell surface. The cell and vesicle membranes fuse and the agent is liberated. The mast cell secretes histamine and other agents that give rise to local inflammatory reactions. The cells of the adrenal medulla liberate the stress hormone adrenaline, and the beta cells in the pancreas insulin. Neher elucidated the secretory processes in these cell types through the development of a new technique which records the fusion of the vesicle(s) with the cell membrane. Neher realized that the electric properties of a cell would change if its surface area increased making it possible to record the actual secretory process. Through further developments of their sophisticated equipment the resolution finally permitted recording of each little vesicle fusing with the cell membrane.
Regulation of Ion Channel Function
Neher and Sakmann also used the electrode pipette to inject different agents into the cell, and they could thereby investigate the different steps in the secretory process within the cell itself (see above). In this way a number of cellular secretory mechanisms have been clarified such as the role of cyclic AMP (see Nobel Prize to Sutherland 1971) or calcium ions. For instance, we now have a better understanding of how the hormone levels in the blood are maintained at a certain level.
Also the basal mechanisms underlying the secretion of insulin have been identified. The level of blood glucose controls the level of glucose within the insulin-forming cell, which in turn regulates the level of the energy rich substance ATP. ATP acts directly on a particular type of ion channel which controls the electric membrane potential of the cell. The change of membrane potential then indirectly influences other ion channels, which permit calcium ions to pass into the cell. The calcium ions subsequently trigger the insulin secretion. In diabetes the insulin secretion is out of order. Certain drugs commonly used to stimulate insulin secretion in diabetes act directly on the ATP-controlled ion channels.
Many other diseases depend entirely, or partially, on a defect regulation of ion channels, and a number of drugs act directly on ion channels. Many pathological mechanisms have been clarified during the eighties through ion channel studies, for instance cystic fibrosis (cloride ion channels), epilepsy (sodium and potassium ion channels), several cardio-vascular diseases (calcium ion channels), and neuro-muscular disorders like Lambert-Eatons disease (calcium ion channels). With the help of the technique of Neher and Sakmann it is now possible to tailormake drugs, to achieve an optimal effect on particular ion channels of importance in a given disease. Drugs against anxiety act for instance on certain inhibitory ionic channels in the brain. Alcohol, nicotine and other poisons act on yet other sets of ion channels.
In summary, Neher and Sakmann's contributions have meant a revolution for the field of cell biology, for the understanding of different disease mechanisms, and opened a way to develop new and more specific drugs.
References
Alberts et al.: The Molecular Biology of the Cell. Garland Press, 1990, 2nd edition, pp. 156, 312-326, 1065-1084.
Grillner, S. I: N. Calder (ed.). Scientific Europe. Foundation Scientific Europe, 1990.
Grillner, S. & Hökfelt, T.: Svindlande snabb utveckling präglar neurovetenskapen. Läkartidningen 1990, 87, 2777-2786.
Rorsman, P. & Fredholm, B.B.: Jonkanaler - molekylär bakgrund till nervtransmission. Läkartidningen 1991, 88, 2868-2877.
The Royal Society of Canada regularly presents the McNeil Medal for the Public Awareness of Science to deserving educators. This year the award was given to Brian Alters of McGill University for his contributions to the teaching of evolution in public schools and universities.
Professor Alters is a member of the board of directors of the National Center for Science Education [see Brian Alters honored by Royal Society of Canada]. He has some wise words about teaching evolution.
The following excerpts are from Brian Alters' book Teaching Biological Evolution in Higher Education: Methodological, Religious, and Nonreligious issues.
Critical thinking—most faculty want students to be critical thinkers. Many students, however, are epistemological duelists, viewing the academic world in terms of true or false, right or wrong, credit or no credit. Instead of analyzing evidence that contradicts their erroneous conceptions, students often just passively receive knowledge from authorities—professors. To become active learners, students need professors to use methods that involve them in grasping the important concepts; but, only 10%-30% of professors use methods other than traditional lectures as their primary pedagogy.
Do these sound like motherhood statements? If you answered "yes" then you aren't paying attention.
Alters is saying that students will readily cope with "information" in a course even if it contradicts their misconceptions. They'll simply make it part of their worldview or, even worse, ignore the fact that it conflicts and spew it back on the exam.
Whether or not students have taken courses in biology or evolution, they come to the science classroom with a variety of memories, knowledge, experience, and evolution conceptions. Often, some of those conceptions are different from scientific concepts. Students develop these conceptions from what they read in the popular press, find on the Web, and see on television and from their interactions with "nature," their peers, and their parents and other authority figures. Instructors at all levels have a complex task: to tap into what students know to assist them in building on their scientific knowledge, to help them replace their misconceptions with scientifically useful conceptions, and to help them construct meaning from their learning experiences.
Helping students construct meaning from their learning experiences is a daunting task. Only the students can do it; instructors cannot "fill" them with knowledge. All instructors can do is to provide learning experiences that facilitates students' generating links between relevant information they already know and new information. From such a constructivist perspective, learning is a social process in which students make sense of experience in terms of what they already know. But how does the professor engineer lessons to help students link the new information with the old in useful, accurate, and appropriate ways? And what happens when the "old" information consists of one or more scientific misconceptions?
What many instructors know from their own classroom experience is that student misconceptions (also called native conceptions, alternate conceptions, intuitive use, prior conceptions, preconceptions, or undesired understandings) are not easily changed. What many people do not realize, however, is that the process of conceptual change takes a long time, perhaps years, depending on the concept, and appears to be an incremental process. In learning evolutionary concepts in particular, students appear to need an extended exposure to and interaction with these concepts for growth in their understanding to occur. Instructors, therefore, may think of the learning experiences they provide for students is only one stepping stone towards the goal of more complete under standing.
To facilitate a constructivist approach in the classroom, an instructor should provide situations in which students examine the adequacy of their prior conceptions, allowing them to argue about and test them. The contradictions students may face during this testing process can provide the opportunity for them to acquire more scientifically appropriate concepts.
What this means is that students carry a lot of baggage into the university classroom. You're not going to change their conceptual understanding of evolution by just presenting the facts are you see them. You're also not going to be successful if you think that just giving them the right concepts—such as the importance of random genetic drift—is all it takes.
In order to start down the path toward changing their misconceptions, you need to directly challenge those misconceptions and bring the conflict out into the open. You need to do this even if you think the misconceptions are based on non-scientific issues.
In other words, teach the controversy.
I agree with Brian Alters on all these points. I disagree with him about some other things and, in one case, I think he makes a big mistake. In all his writings he assumes that student misconceptions need to be addressed and university instructors only need to learn which methods are most effective. In my opinion, he doesn't pay enough attention to the fact the instructors also have misconceptions that need to be corrected.
The molecule is the potassium ion channel from rat brain cells. Roderick MacKinnon solved this structure and he got the Nobel Prize in 2003 for his work on the structure and function of the potassiunm ion channel [see Nobel Laureat: Roderick MacKinnon]
The Nobel Laureates for this week are Erwin Neher and Bert Sakmann for working out a technique to measure the voltage changes during ion transport.
The winner is Dima Klenchin of the University of Wisconsin, Madison.
Identify this molecule. Be as specific as possible. Briefly describe what it does
There's a Nobel Prize indirectly connected to this molecule. The prize was for developing a technique that could be used to study the function of molecules like this one.
The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.
There are only five ineligible candidates for this week's reward: Ben Morgan of the University of North Carolina at Chapel Hill, Frank Schmidt of the University of Missouri, Joshua Johnson of Victoria University in Australia, Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, and Jason Oakley a biochemistry student at the University of Toronto.
Frank and Joshua have agreed to donate their free lunch to an undergraduate. Consequently, I have an extra free lunch for a deserving undergraduate so I'm going to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.
THEME:
Nobel Laureates Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.
Correct responses will be posted tomorrow.
Comments will be blocked for 24 hours. Comments are now open.
One of the problems with adaptationist just-so stories is that they often sound so plausible that everyone just assumes they must be true and stops thinking critically. One of the classic examples is the adaptationist explanation of menopause.
The "Grandmother Hypothesis" says that menopause arose in primitive hominids because it prevented pregnancies in older women thereby freeing them to assist in the care of their grandchildren. This extra care had a significant effect on the survivability of the grandchildren thereby increasing the probability that the frequency of the menopause allele would increase in the population.
Over the course of thousands of generations, the allele for menopause became fixed in our ancestral populations because it conferred a significant adaptive advantage.
Razib Khan believes in this adaptationist explanation for menopause. He quotes from a recent study that seems. on the surface, to lend support to the idea. See the recent posting on Gene Expression: Menopause as an adaptation.
The study by Virpi Lummaa looked at the presumed benefit of grandmothers among Finnish families. She reports that children with the support of a grandmother are 12% more likely to survive than children without such support.
The prompts Razib to write.
12% is a very big effect and would lead to rapid evolutionary change (on the order of thousands of years in the most simple population genetic model of a single locus of dominant effect).
I posted a comment on his blog. I'm reproducing it here in order to get more feedback.
12% is, indeed, a very large effect but what does it have to do with evolution?
We're looking at a study where every single woman underwent menopause so one of the things we certainly aren't doing is testing to see whether menopause has an effect on the survivability of grandchildren.
Let's think about reasons why some families have grandmothers to help out and some don't. First, there's the relative proximity of living grandmothers. Then there's the question of the relationship between parents and grandparents. Let's not forget possible financial help that has nothing to do with direct caregiving. Finally, there's the issue of whether a family even has a surviving grandmother.
None of theses things are affected in any way by the fertility or non-fertility of the grandmother, right? The 12% difference has nothing to do with menopause.
Now let's think about a time in the past when menopause was presumably evolving. You had two kinds of females in the population, those who underwent menopause and those who didn't. There will still be all kinds of families who experience the help of a grandmother irrespective of whether she can still have kids or not. That's the background that a presumed adaptation has to deal with.
If there are non-menopausal women who live into their fifties, are close to their grandchildren, and whose husband is dead, then they will presumably help raise thier grandchildren. Same thing applies to non-menopausal women who simply don't risk getting pregnant any more even though their spouse is alive. (Just say "no." It's probably more common than you think. Women are not stupid.)
In fact, the adaptationist just-so story only really applies to that small subset of women who have the following characteristics.
They live past 50 years old.
They have grandchildren who are young and still need care.
They don't have too many grandchildren in different families so their caregiving can be effective.
They live near their grandchildren and can help out.
They have a good relationship with their children and their spouses.
Their husbands are still living.
They choose to get pregnant.
That's the only group that menopause affects. It eliminates #7 but has no effect on any of the other factors. It certainly doesn't have any effect on whether the grandmother was dead or alive at 50 years old.
Given that there were many families that received no help from grandmothers, whether they had the menopause allele or not, and given that there were many families who received help even if the grandmothers did not have the menopause allele, the question is "what is the adaptive value of menopause under those circumstances."
What does the Lummaa study have to say about that?
Since you are a supporter of this adaptationist explanation can you describe for me the kind of society where you think this allele became fixed in the population? Was it a hunter-gather society of small bands or a large agricultural society of small towns? Or something else?
I'd like to hear more details about how this grandmother hypothesis actually worked in Australopithicus or Homo erectus societies. Please include your estimate of how many grandmothers survived past the age where menopause could make a difference as you estimate the fitness coefficient.
[Image Credit: "Rudyard Kipling’s illustration for The Elephant’s Child from Just So Stories (1902)." From Encyclopedia Britannica
Identify this molecule. Be as specific as possible. Briefly describe what it does
There's a Nobel Prize indirectly connected to this molecule. The prize was for developing a technique that could be used to study the function of molecules like this one.
The first person to identify the molecule and name the Nobel Laureate(s) wins a free lunch. Previous winners are ineligible for six weeks from the time they first won the prize.
There are only five ineligible candidates for this week's reward: Ben Morgan of the University of North Carolina at Chapel Hill, Frank Schmidt of the University of Missouri, Joshua Johnson of Victoria University in Australia, Markus-Frederik Bohn of the Lehrstuhl für Biotechnik in Erlangen, Germany, and Jason Oakley a biochemistry student at the University of Toronto.
Frank and Joshua have agreed to donate their free lunch to an undergraduate. Consequently, I have an extra free lunch for a deserving undergraduate so I'm going to award an additional prize to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch. If you can't make it for lunch then please consider donating it to someone who can in the next round.
THEME:
Nobel Laureates Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule(s) and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.
Correct responses will be posted tomorrow.
Comments will be blocked for 24 hours. Comments are now open.
A Day of General Thanksgiving to Almighty God for the bountiful harvest with which Canada has been blessed … to be observed on the 2nd Monday in October.
The modern holiday dates from about one hundred years ago and it is heavily influenced by the American tradition that was beginning to become well known at that time.
However, the original celebration clearly descends from harvest festivals celebrated in Europe hundreds of years ago. The first Europeans to come to North America brought this celebration with them and it likely became more popular because several East coast aboriginal tribes celebrated a harvest festival.
Canada claims that the first thanksgiving in North America was in 1578 when Martin Frobisher organized an autumn celebration in Newfoundland.1 Samuel de Champlain frequently celebrated thanksgiving feasts in the early French colonies in Nova Scotia and Quebec beginning in 1604. The local natives joined in these celebrations [see L’Ordre de Bon Temps (Order of Good Cheer)].
Further south, the English settlers in New England began to celebrate a harvest festival in 1621. A tradition that they brought with them from Europe. It's this version of the English festival that has come down to us as the prototypical thanksgiving day. That part of the tradition was imported to Canada in the late 1700s when thousands of settlers fled north from the new United Sates of America to take up residence in the British Colony of Canada.
1. The other contender is a festival on September 8, 1565 in Saint Augustine, Florida. Is Florida part of North America? :-)
Some people in the intelligent design community don't like it when we refer to their beliefs as "Intelligent Design Creationism." They claim they aren't creationists when they talk about an intelligent designer who createdspoke designed life.
Nick Matkze got involved in a discussion with one of those people. It's worth reading his comments on Panda's Thumb: The truth hurts. Check out the comments as well. The posting pretty much covers the main issues in the debate.
As usual, the Intelligent Design Creationists (a.k.a. IDiots) don't have a rational leg to stand on.
I'll just post this without comment because I can't, for the life of me, figure out the logic [Denyse O'Leary on Uncommon Descent; Serving the Intelligent Design Community: Off topic: Single payer health care]
Here I was recently treated to an interesting display of Darwinist logic.
A commenter demanded that I provide proof that in a single-payer health system like Canada’s, older people are being abandoned to die. Another suggested I just shut up about it.
Sorry. Go here for how bad it can get.
It’s a matter of simple logic, really. Sarah Palin’s death panels are alive and well in Canada because we have a single government payer health system.
I believe that universities are special places. The primary objective of the university community is to learn and investigate. That goal should not be restricted or impeded by outside concerns, especially if those "concerns" are ideologically or politically motivated. Society relies on universities to harbor unconventional and unusual opinions. It's where the minority viewpoint can be protected until it becomes the majority, as happens so often in a progressive society.
The other objective of a university is disseminating knowledge. That's why students come to a university to learn and it's why universities offer public lectures. It's why students and faculty members are encouraged to speak out on controversial topics. Universities thrive on diversity and that's why the most extreme opinions can be heard on campuses. It's part of the deal.
We're all familiar with the attempts to censor unpopular opinions. Mostly we get upset when left-wing protests are suppressed as happened during the 60s when the anti-war demonstrations were opposed [see Kent State Shootings]. We know about attempts to fire communist and gay professors and we are outraged to learn that women are being discriminated against in the universities.
What about opinions that don't fall into the liberal camp? Are we upset when those opinions are suppressed in the universities? No, not so much. I'm constantly surprised and disappointed when I hear some of my colleagues urging the dismissal of creationist professors or trying to block IDiots from lecturing on campus.
That's stupid and hypocritical. The value of a university is only protected when all opinions are respected.1 You can't pick and choose which ones deserve protection and which ones should be censored. Universities don't function once you start down that path.
The McGill student newspaper has started down that path with an article about a student pro-life club: EDITORIAL: Choose Life crossed the line with Ruba event. The editors seem to have set themselves up as sole arbitrators of some kind of imaginary "line" that can't be crossed.
At 6 p.m. tonight, Choose Life, the Students' Society's pro-life club, will host a presentation by Jose Ruba, a co-founder of the Canadian Centre for Bio-Ethical Reform, titled "Echoes of the Holocaust." Ruba's speech will attempt to draw parallels between abortion and the Holocaust, by arguing that "dehumanization and denial of personhood has justified some of the greatest affronts to human dignity that the world has seen." The presentation refers to abortion as a "mass human rights violation" and includes graphic imagery such as photos of dead bodies at concentration camps followed by photos of supposedly aborted foetuses.
On Thursday night, SSMU Council voted to censure the event and to make Choose Life ineligible to receive funding if they go through with tonight's presentation. We commend them for that decision. The comparison of abortion to the Holocaust is not only horribly offensive and inaccurate, it is deliberately designed to be inflammatory. This event is not intended to foster debate - it is designed to be provocative and to distract from meaningful discussion of abortive rights.
These are the sorts of issues that test our mettle. Either you support freedom of expression on the campus or you don't. There's no middle ground where you support some expression but not others.2
The editors of The McGill Tribune have just failed the test.
The SSMU Executive is incredibly concerned and upset about the response of McGill University to the recent "Echoes of the Holocaust" event, hosted by the SSMU club Choose Life. We feel that McGill University has not only disrespected the rights of the SSMU as the accredited representative body of all McGill undergraduate students, but also failed to protect students' rights.
McGill University has not respected SSMU Council and the SSMU Executives as representatives of the McGill undergraduate student population. When the SSMU Council passed a resolution officially and publically censuring the event "Echoes of the Holocaust", the SSMU Council clearly stated that for Deputy Provost (Student Life and Learning) Morton Mendelson to permit it to go forward would disregard the desire of the Council. In response Professor Mendelson argued that this resolution is a tyranny of the majority. Firstly, this is an offensive misrepresentation of the purpose of SSMU Council. The SSMU Council was acting on behalf of all undergraduate students, both in its representative capacity and in reaction to many conversations with students. Secondly, it is worrisome that the Deputy Provost interprets a large percentage of students being outraged and appalled at an event to be a tyranny of the majority. The SSMU had hoped that he would consider the impact as well as content of the presentation instead of ignoring the formal intervention of students' representative body by using the rhetoric of academic freedom.
So we're reduced to the point where academic freedom is just "rhetoric"?3
I remember the days when it was students who were advocating freedom of expression and administrators who were trying to suppress it. Now those students are administrators and we have a whole new generation of students who don't understand the meaning of freedom on a university campus. How times change.
Incidentally, a large group of students succeeded in preventing Jose Ruba from speaking at the event according to a report in The National Post: Tim Mak: McGill abortion advocates block opposing opinions. They sang songs for three hours until the organizers gave up and went home.
Here's a video of the first part of the event so you can see for yourselves what transpired. The students do not earn my respect for their behavior. They have the right of freedom of expression and they have the right to express their disagreement but they do not have the right to prevent contrary opinions from being expressed on a university campus.
The event prompts Tim Mak, a former employee of the Fraser Institute, to write ...
But these are university campuses nowadays, ruled by an arrogant minority on the left, who despite their paucity, believe they speak for everyone. "I don't think that this type of talk should be allowed to happen at McGill," said Eisenkraft Klein, one of the protestors arrested, in the McGill Tribune. "This is student space. This is not public property."
What conceit. Klein’s implication was that her opinions represented those of all McGill students, that student space was only for activities that conformed to her parochial political views. I’m by no means a supporter of the pro-life movement. But I am a supporter of the modern conservative movement – a movement that believes that freedom of speech means free speech for all. On the other hand, the left has found it convenient to hide behind the tenets of free speech when they want to, say, condemn Israel, but have found it much harder to extend the protections of free speech to positions they disagree with.
I’ve always found that the most interesting lecturers are those with whom I have the least in common. Who wants to spend a couple hours nodding affirmatively at PowerPoint slides? But we’ll never know what Ruba might have said, and all reasonable students have left to do is sing the free speech blues.
Some of you might be afraid that the world is coming to an end when I agree with someone like Tim Mak. Not so, there really are open-minded conservatives who defend freedom of expression. I'm proud to ally with them on this issue.
Call me an accommodationist ...
A good case can be made that exposing stupid ideas to the light of day—and to serious debate in the university community—is the best way to discredit them. (Ignoring them works, too.) Trying to suppress them is the best way to give them the publicity they thrive on and it has the exact opposite effect to what the protesters desire. So, in addition to objecting to the student's behavior on the grounds of protecting freedom of expression, I object on the grounds that it's a tactically stupid way to oppose kooks.
1. "Respected" doesn't mean you have to agree. You can vigorously oppose any idea that's expressed on a campus but you can't muzzle it on the grounds that you disagree.
2. Don't quibble about this. Yes, we can all think of some examples of expression that must be excluded—yelling "fire" in a crowded classroom—for example.
3. I'm aware of the fact that the term "academic freedom" can be misused. If Morton Mendelson used "academic freedom" to permit the event to go forward then that's unfortunate. There are better ways to describe the principle I defend—it's "freedom of expression on university campuses."
[Hat Tip: Canadian Cynic. I strongly disagree with him on this one.]
Here's a chart of the average annual global temperature change over the past 150 years. I don't know about you, but to me there seems to be a bit of a trend.
The highest recorded temperature was in 1998 and last year the temperature was 0.08° lower than the year before. Nobody with an IQ over 50 thinks that the temperature has to increase every single year in order to demonstrate global warming.
This headline may come as a bit of a surprise, so too might that fact that the warmest year recorded globally was not in 2008 or 2007, but in 1998.
But it is true. For the last 11 years we have not observed any increase in global temperatures.
And our climate models did not forecast it, even though man-made carbon dioxide, the gas thought to be responsible for warming our planet, has continued to rise.
So what on Earth is going on?
It's actually not quite as bad an article as it sounds. There's some interesting discussion about short-term trends and how to predict them. Unfortunately the author leaves the impression that global warming may not be caused by humans. In seven of the past eight years the global temperature has been higher than it has ever been except for 1998. Isn't that worth mentioning?
The interesting thing about this is that the exact quotation above is presented on Uncommon Descent under the same scary title: What happened to global warming?. There's no additional information to put the headline into context.
Why is there a correlation between the rejection of evolution and the rejection of other scientific discoveries? Isn't it obvious? The IDiots are not in the business of promoting the scientific theory of Intelligent Design Creationism. Their goal is to discredit science and they'll try anything at all to advance that goal.
The pathway of information flow runs from DNA to RNA to proteins. There are a bunch of fundamentally important steps in this pathway including transcription, RNA processing, and translation. 
Thanks to this year's Nobel Laureates, and Harry Noller, we now know the structure of the ribosome at the molecular level and we know where the tRNAs and the translation factors bind. 
The 2009 Nobel Prizes provide science writers with an excellent opportunity to highlight some discoveries that are really important in biology. You'd think that science writers would be all over this.
