Bjørn Østman

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Pleiotropy
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  • November 9, 2008
  • 12:00 AM
  • 1,606 views

Head injury as a cause of ADHD

by Bjørn Østman in Pleiotropy

Head injury is not a causative factor of ADHD, but it may be a marker for subsequent diagnosis of ADHD.... Read more »

  • October 10, 2008
  • 12:00 AM
  • 1,589 views

Non-functional DNA conserved in evolution

by Bjørn Østman in Pleiotropy

When a stretch of DNA is really important for an organism, natural selection will make sure that it is not changed much from generation to generation. This is termed purifying selection, and whenever it is observed, the conserved DNA is responsible for some function that the organism can't do without.Conversely, when a stretch of DNA is observed to code for an important function in the organism, it is a pretty solid guess that it is highly conserved by purifying selection. Survival and/or reproduction is difficult* without the function, so any changes to that DNA is not tolerated by natural selection.There are many examples of this, so there is not a lot of contention over this issue. I mean, there isn't any, at all.But now two guys at Stanford University has come along and destroyed this pretty picture. McLean and Bejerano have in mice discovered ultraconserved non-exonic elements (stretches of DNA that do not code for a protein), which do not cause a phenotype when deleted (source). In other words, while this DNA is highly conserved, showing strong purifying selection during the evolutionary history of mice, the mice seem to do fine without it. It doesn't seem to serve any function that the mouse can't do without. Astonishing!What is going on? Surely this DNA must be doing something? McLean and Bejerano will now make a thorough investigation into the matter, and hopefully unravel this mystery. One suggestion is that the ultraconserved DNA plays a role under some circumstance that the mice are not subject to in the laboratory. After all, the sheltered life of a lab mouse is quite different from that of wild mice. Any number of environmental conditions that are in effect outside the lab and not inside could explain the necessity. Pathogens, perhaps? It turns on expression of genes that produce a venom when the mice are eaten, maybe? Could it be that it is involved in some higher cognitive function that only Douglas Adams knew about?McLean, Bejerano (2008). Dispensability of mammalian DNA Genome Research* I know, I know. This is Mission Impossible. Difficult should be a walk in the park.... Read more »

McLean, Bejerano. (2008) Dispensability of mammalian DNA. Genome Research.

  • November 5, 2008
  • 12:00 AM
  • 1,570 views

Homosexuality is catholic in the animal kingdom

by Bjørn Østman in Pleiotropy

Beetles, bisons, black swans, bonobos, dolphins, elephants, flamingos, fruit bats, fruit flies, giraffes, lions, lizards, macaques, orangutans, ostriches, penguins, sheep. What do these animals have in common?They are all homosexual. In fact, the list is much, much longer. Here is what Petter Bøckman has to say about it:No species has been found in which homosexual behaviour has not been shown to exist, with the exception of species that never have sex at allWe can thus safely conclude that the argument against human same-sex marriage - that homosexuality is not natural - is invalid. If we wish to be informed by nature in this matter, proposition 8 should not have been passed (but of course, those who are against same-sex marriage are either homophobic or religious - they don't really care if it's natural or not).In fact, I personally find this little story quite touching:Roy and Silo, two male chinstrap penguins at New York's Central Park Zoo have been inseparable for six years now. They display classic pair-bonding behavior—entwining of necks, mutual preening, flipper flapping, and the rest. They also have sex, while ignoring potential female mates.The question then is why animals are homosexual at all. As reproduction really only does occur between male and female, it would seem evolutionarily disadvantageous to spend any time sexing up to members of your own sex. Lost effort. So why do it?There are a number of hypotheses trying to explain the phenomenon. It could be to establish social dominance. I have heard this is the case with orangutans, where the dominant male will take the loser after a fight. It could be practice for prom night. Could even be that sperm is deposited on the other male, who then injects it into the next female he gets frisky with. Social cohesion is another possibility (which is ironic, because religion has also been posited to boost social cohesion). This is most probably the case in bonobos: 75 percent of bonobo sex is nonreproductive and that nearly all bonobos are bisexual (source).These are all adaptive reasons for homosexuality. But there are non-adaptive possibilities too. Generally, it could be a by-product of another trait that is adaptive. It could be a developmental anomaly, such as an enlarged sexually dimorphic nucleus in the ovine medial preoptic area (source).Last month a paper came out in the Journal of Evolutionary Biology (reference below) in which the authors suggest that homosexual copulations may be a behavioural mechanism that allow males to expel older, potentially low-quality sperm (reader-friendly report in National Geographic). The authors investigated the "dominance", "practice", and "sperm translocation" hypotheses mentioned above in flour beetles (Tribolium castaneum), but found no evidence for the first two, and only little for the third. Instead, based on direct observation of flour beetle sperm ejaculated upon another male, the researchers conclude that the beetles seem to use homosexual copulatory behavior to get rid of inferior spermatophores.I find this hypothesis intriguing, but I really don't think there is enough evidence to conclude that flour beetle homosexuality serves such a mundane purpose. Without having to invest any time in such research, I would bet that this behavior is maintained in evolution because it feels good, which sex most probably often does for adaptive reasons. And as long as the males that indulge with other males also do it with females, the behavior need not be lost in evolution.If the males are only so good at telling males and females apart, the fittest males may be those who don't think twice about who they get behind. Imagine this algorithm:1) Find another beetle.2) Mate with other beetle.3) Check gender of other beetle.4) Goto 1.Depending on how easy step 3 is, that might be way more adaptive than this one:1) Find another beetle.2) Check gender of other beetle.3) If other beetle is female, copulate.4) Goto 1.K. E. LEVAN, T. Y. FEDINA, S. M. LEWIS (2008). Testing multiple hypotheses for the maintenance of male homosexual copulatory behaviour in flour beetles Journal of Evolutionary Biology DOI: 10.1111/j.1420-9101.2008.01616.x... Read more »

  • March 10, 2009
  • 12:00 AM
  • 1,548 views

Chimpanzee plans for the future

by Bjørn Østman in Pleiotropy

Santino is a thirty year old male chimpanzee at Furuvik Zoo in Sweden. For the last decade he has been collecting stones before the zoo opens, stashing them in around his enclosure, and then when the visitors arrive, has been throwing the rocks at them - though, thankfully, he apparently has a poor aim.... Read more »

  • December 26, 2008
  • 12:00 AM
  • 1,542 views

Neanderthals outcompeted by humans?

by Bjørn Østman in Pleiotropy

Wouldn't you love it if the Neanderthals hadn't gone extinct, but were still living with us today? I'd give my right arm to see that (but then again, I'd give my right arm to be ambidextrous). It is still hotly debated how they went extinct, but a paper in PLoS ONE [1] concludes that Homo neanderthalensis were outcompeted by humans.... Read more »

William E. Banks, Francesco d'Errico, A. Townsend Peterson, Masa Kageyama, Adriana Sima, & Maria-Fernanda Sánchez-Goñi. (2008) Neanderthal Extinction by Competitive Exclusion. PLoS ONE, 3(12). DOI: 10.1371/journal.pone.0003972  

R GREEN, A MALASPINAS, J KRAUSE, A BRIGGS, P JOHNSON, C UHLER, M MEYER, J GOOD, T MARICIC, & U STENZEL. (2008) A Complete Neandertal Mitochondrial Genome Sequence Determined by High-Throughput Sequencing. Cell, 134(3), 416-426. DOI: 10.1016/j.cell.2008.06.021  

  • December 29, 2008
  • 12:00 AM
  • 1,497 views

Go on, marry your cousin

by Bjørn Østman in Pleiotropy

Not that I was ever thinking about it, but should I marry my cousin? Should anyone? Is it such a bad idea that there should be laws against it? You may not know that there are laws prohibiting first cousins from marrying in most US states. In this picture the white colored states are the ones that do not.... Read more »

  • January 30, 2009
  • 12:00 AM
  • 1,472 views

Finger lengths predict stockbrokers' success

by Bjørn Østman in Pleiotropy

Longer ring fingers predict how well stockbrokers do at trading in fast-paced high-risk markets.... Read more »

J. M. Coates, M. Gurnell, & A. Rustichini. (2009) Second-to-fourth digit ratio predicts success among high-frequency financial traders. Proceedings of the National Academy of Sciences, 106(2), 623-628. DOI: 10.1073/pnas.0810907106  

  • January 18, 2009
  • 12:00 AM
  • 1,412 views

Wealthy men's women have more orgasms

by Bjørn Østman in Pleiotropy

If your man is rich you'll have a higher frequency of orgasms. At least if you're Chinese (not including Tibet and Hong Kong). Why is this interesting at all, except that it's about sex, which human find interesting in a of itself? Well, because we have no idea why women have orgasms in the first place. It pretty clear why, and notably when, men have orgasms, but no one really knows why women have them.Male income and height are were included to measure male quality, because both parameters have previously been found to affect male reproductive success. Rich men are sexy. Tall men are sexy. But does male sexiness translate into more female orgasms?The hypothesis about female orgasms that Pollet and Nettle investigate is this one.If female orgasm is adaptively designed for discriminating male quality, then it should be more frequent in females paired with high-quality males. And since male quality is wealth and height, their prediction is clear.If the adaptive view of female orgasm is correct, then we predict that women will report more frequent orgasms the richer their partners are and the taller their partners are.The 1534 women in the study self-reported via computers away from the their homes, so if you think you can trust self-reporting (which is always an issue), you may agree with the authors that women have more orgasms the higher their partner's income is. But does this explain why women have orgasms at all?They end the paper thus.The data produced so far, while apparently consistent with an adaptive role for female orgasm, are far from definitive. Moreover, even if consistent with an adaptive role for female orgasm, these data do not allow conclusive testing between two alternative proposed functions—namely, that female orgasm differentially promotes emotional bonding with high-quality males or that it differentially promotes conception with such males under conditions of sperm competition.More research is need to elucidate the function of the female orgasm. Anyone disagree with that?Additionally, there was a slight trend that partner height influence orgasm frequency the same way that wealth does. The probability that this was a random effect was 0.5<p<0.1, meaning that it didn't quite make below the magical P-value of 5%. We definitely need more data on that.Reference:T POLLET, D NETTLE (2009). Partner wealth predicts self-reported orgasm frequency in a sample of Chinese women Evolution and Human Behavior DOI: 10.1016/j.evolhumbehav.2008.11.002... Read more »

  • February 18, 2009
  • 12:00 AM
  • 1,381 views

Plants are officially boring

by Bjørn Østman in Pleiotropy

This fantastic paper finally proves that plants are boring and animals are exciting. At least in the eyes of men.... Read more »

  • April 2, 2009
  • 12:20 AM
  • 1,369 views

Amazonian tribe is from another planet

by Bjørn Østman in Pleiotropy

A society so strange it changes what it means to be human. A culture so foreign that the ways which we know ourselves are altered. I no longer need to invoke aliens coming to Earth to imagine how one culture might find another extraterrestrial. The Pirahã will do.... Read more »

  • August 6, 2009
  • 10:17 PM
  • 1,329 views

Darwin's theory can handle the landscape

by Bjørn Østman in Pleiotropy

Cue the fitness landscape. A multi-dimensional function for organism fitness (ability to reproduce) as a function of the genotype*. A population moves "uphill" when it can to maximize fitness, akin to physical systems, which always moves to minimize its energy.... Read more »

Weissman DB, Desai MM, Fisher DS, & Feldman MW. (2009) The rate at which asexual populations cross fitness valleys. Theoretical population biology, 75(4), 286-300. PMID: 19285994  

  • October 7, 2008
  • 12:00 AM
  • 1,289 views

Evolution and pleiotropy

by Bjørn Østman in Pleiotropy

Pleiotropy is the effect of one gene affecting multiple traits, as when Drosophila genes are expressed in more than one place during embryogenesis. For a bunch of examples of that, seeRepression and loss of gene expression outpaces activation and gain in recently duplicated fly genes, Oakley, Østman, and Wilson, 2006, PNAS, 103, 11637.In my own work on computer simulations of epistatic interactions, it is clear that pleiotropy has the effect of changing the phenotype more per mutation than withoput pleiotropy. With pleiotropy, more than one trait gets affected by each mutation. And each trait can potentially be affected by the same amount (i.e. numerical value), so if a mutation affects five instead of one trait, it can change the fitness five times as much. Admittedly, this is a result from simulating a very simple model, but that it has biological relevance is suggested (among other considerations) in a recent Nature paper by Günter Wagner et al. where they measure pleiotropy in mice. They show that a substitution at a QTL has an effect on each trait that increases with the total number of traits affected. While mutations in many genes produces only a small effect on a few traits, those that affect many traits does so with higher effect.Pleiotropic scaling of gene effects and the ‘cost of complexity’, Wagner, Kenney-Hunt, Pavlicev, Peck, Waxman, Cheverud, 2008, Nature, 452, 27.The significance of this observation is that once the environment changes, and the population is forced to adapt, those organisms that exhibit much pleiotropy in the genomes can adapt really fast. And that organisms can adapt way faster than we normally imagine became increasingly clear when a paper came out this year about a lizard, Podarcis sicula. This lizard evolved differences in head morphology, bite strength, and digestive tract structure in a very, very short period of time. How short? Ten thousand years? That would be short by evolutionary standards. But no, it just took 36 years! In about 30 generations the lizards evolved larger heads, stronger bites, and cecal valves - a structure in the gut that can constrict, slowing dowen the passage of food, giving more time for digestion. Behaviorally the lizards changed their diet to include much more plant material, and the morphological changes were adaptations to this new lifestyle. Clearly the lizards became a new species, as they moved into a new niche. You can read more about that all over the web - it deservedly got a ton of coverage - but I recommend Science Daily for this one.Herrel, Huyghe, Vanhooydonck, Backeljau, Breugelmans, Grbac, Van Damme, and Irschick (2008). Rapid large-scale evolutionary divergence in morphology and performance associated with exploitation of a different dietary resource PNAS, 105 (12)... Read more »

  • January 20, 2009
  • 12:00 AM
  • 1,283 views

Evolution does mean better and more complex

by Bjørn Østman in Pleiotropy

The American Society of Human Genetics has a quick little quiz on evolution. Unfortunately they get one question wrong about 'evolution' implying 'better' and 'more complex'.... Read more »

Claus O. Wilke, Jia Lan Wang, Charles Ofria, Richard E. Lenski, & Christoph Adami. (2001) Evolution of digital organisms at high mutation rates leads to survival of the flattest. Nature, 412(6844), 331-333. DOI: 10.1038/35085569  

Christoph Adami. (2002) What is complexity?. BioEssays, 24(12), 1085-1094. DOI: 10.1002/bies.10192  

  • October 6, 2008
  • 12:00 AM
  • 1,226 views

Natural Selection Fails to Optimize Mutation Rates

by Bjørn Østman in Pleiotropy

Rich Lenski's group published this paper in PLoS Computational Biology less than two weeks ago:Clune J, Misevic D, Ofria C, Lenski RE, Elena SF, Sanjuán, R. (2008). Natural Selection Fails to Optimize Mutation Rates for Long-Term Adaptation on Rugged Fitness Landscapes. PLoS Comput Biol 4(9). PLoS Computational Biology, 4 (9).In the Ph.D. program I'm in we are required to give a journal club talk once per semester (the result of which is that that's exactly how many we give), and I chose to do this one for last Wednesday because it is something I worked on briefly in the NK-landscape a while back*.Clune et al. used AVIDA to investigate if natural selection is sufficient to evolve mutation rates that are close to the static mutation rates that optimize fitness. First they do a bunch of runs with different mutation rates to find which one optimizes fitness, and find a genomic mutation rate of Uopt=4.641 (figure 1). Then they allow the value of the mutation rate to change by mutation, and compare the evolved mutation rates and resulting fitness to that of the static ones. They find that the evolved mutation rate is much lower than Uopt, and that the average population fitness is also much lower than that obtained for Uopt. In other words, a population left to evolve by natural selection does not evolve a mutation rate that benefits the population the most.Figure 1: Population average fitness of with static mutation rates (solid black line) compared to evolving mutation rates (red and blue dots). Initial conditions were U=1 (red) and U=10-3 (blue).Their hypothesis to explain this puzzling observation is that selection against the mutational load wins over the adaptive benefit of a high mutation rate. When a population sits on top of a local peak in the fitness landscape, it has two choices: Either evolve a low mutation rate, so that it avoids deleterious mutations, which lowers the average population fitness, or it evolves a high mutation rate, so that it can locate another higher peak somewhere not so far away in genotype space. Their result suggest that the former strategy wins. The short-term effect of minimizing the mutational load wins over the long-term benefit of adaptation.They then went on to hypothesize that it is the topology of the fitness landscape the decides which of these alternatives wins. In AVIDA the fitness landscape is very rugged, meaning it has many fitness peaks and valleys. They therefore constructed an explicit landscape in which they could manually adjust the size of a valley that the population would need to cross in order to adapt. Since adaptation is fast, they also switched the landscape every 300 generations between two "seasons" (figure 2). This has the effect of needing more beneficial mutations to optimize fitness, resulting in a longer time of adaptation (which leads to better statistics). As can be seen in this figure, when there is no valley, the population does indeed evolve a mutation rate identical to the static optimal mutation rate. But with a valley size of 2 or 3, both the mutation rate and the resulting fitness is lower than that of a population with the optimal static mutation rate.Figure 2: Explicit fitness landscapes. First and second column show how the fitness landscape alternate between the two "seasons". The third column is the reulting fitness as a function of the mutations rate. Solid line are static mutation rates, and red and blue points are for simulations with evolving mutation rates. The greater the valley is, the harder is is for natural selection to evolve the optimal mutation rate, and it thus fails to optimize fitness when the landscape is rugged.What does that mean for us? For one thing is means that when using evolutionary algorithms to find solutions to human problems we need to be careful setting the mutation rate so that optimal solutions are found.It also suggest there is a barrier preventing real populations of living organisms to optimize their reproductive output when their mutation rates can evolve. Mutation rates do vary between species and individuals. When errors are made by the DNA copying machinery during meiosis and mitosis, there are ways to correct for it. How well that is done depends on proteins that are products of genes, that themselves are prone to copying-errors. It is practically impossible to attain a 100% fidelity (i.e. zero mutation rate), but it is in principle straightforward to select for a machinery that allows more mutations to slip through uncorrected. But alas, the landscape dictates the dynamics and prevents high mutation rates.* In the NK-landscape I found that I could only avoid fixation of a mutator-lcous with zero mutation rate by updating the environment every ten generations. This has the effect of requiring the population to continuously adapt. This was for K=3, which means there is a fair amount of epistasis - the landscape has many local peaks.... Read more »

  • April 23, 2009
  • 08:00 AM
  • 1,224 views

Evolution-proof malaria control

by Bjørn Østman in Pleiotropy

In treating malaria it is crucial to understand evolutionary dynamics. The problem with insecticides such as DDT is that it kills mosquitos (Anopheles) almost immediately after contact, and thus imposes very strong selection for resistance against the insecticide. The mosquitos evolve resistance within a few years, rendering the whole population immune and the insecticide worthless.... Read more »

  • December 8, 2008
  • 12:00 AM
  • 1,215 views

Graham's cancer selection is without merit

by Bjørn Østman in Pleiotropy

Via a Google advertisement entitled "Evo-Devo" needs "Onco" I found my way to the website of a James Graham. He wrote a book that he published himself in 1993: Cancer Selection: The New Theory of Evolution.Warning: verbose!On his website he writes of himself in the third person:He postulates that cancer killed uncountable numbers of immature animals and concludes that the resulting accumulation of defenses against the disease enabled the emergence of complexity. In all evolving animal lineages selection favored utmost precision in the construction of all cells in order to avoid death of the organism from imprecision in a single cell. This imperative of exactness at the level of individual somatic cells permitted the emergence of complex tissue, organs and organisms.Geoff Watts tells the story of a senior executive in a large multinational corporation who in a flash of inspiration turned himself into an evolutionary biologist. His idea was this.Cancer is a common occurrence, and certainly a life-threatening one. But biologists generally regard it as having no effect on evolutionary change because it mostly afflicts people beyond their child-bearing years. As a result, cancer cannot affect their chances of passing on any protective genes they may possess to the next generation.I agree that cancer is not without effect. Cancer kills the baby; baby doesn't get to reproduce. But that this should be a driving factor in the evolution of complex tissue etc. needs further elucidation. I have not read his book, and I shall not promise to do so, either. But kick me if Graham has scientifically assessed his hypothesis, you know, like a proper scientist. I mean, if he wants to be taken seriously, this is what he has to do. (Scroll down to learn what he thinks of that idea.)It could serve to eliminate those individuals who inherited a genetic programme unable to cope with any damaging side-effects associated with change. Cancer, in other words, is evolution's method of quality control.But organisms don't need anything to kill them in order to make sure that they don't mature and reproduce. The damaging side-effects - whatever they may be - are enough in themselves. The damaging side-effects is already quality control. Either you make or you don't. In that light there is nothing special about cancer. If your developmental program fail and you get cancer, then you will be selected against. If, say, your immune system fails, then you will be selected against. There is no difference.Childhood cancer kills before the age of reproduction, and is therefore amenable to selection. Yet it continues to exist. Why? Because natural selection has not yet had the time to deal with it.No. Cancer is not one disease. The phenomenon of uncontrolled cell-growth is incredibly varied and thus very, very difficult to evolve resistance to. That alone is a far more parsimonious explanation for the persistence of cancer in children, and thus preferred over Graham's hypothesis.And hypothesis is apparently all we get, because Graham is outright against testing his idea scientifically:Graham claims that cancer selection is not a but the driving force in the emergence of complex animal life. "He believes that with good, clear thinking one can arrive at an answer," Leroi says. "But this isn't enough.Because something could be a certain way doesn't mean that it actually is that way. All those biologists who spend their time trying to test evolutionary theory - well, he thinks they're just number-crunchers who can't see the big picture." (My emphasis.)Exactly!Graham has also written a document listing twenty-five problems not solved by conventional evolutionary theory (tl;dr). One of the points goes as follows:5. There is on display at the American Museum of Natural History in New York a fossil of a small disk-shaped jellyfish which is more than 500 million years old. A specialist might detect differences between this fossilized organism and modern specimens, but even experts would agree that the primordial jellyfish looks substantively like today's jellyfish. It seems that, compared to bilaterians, there has been little organismic transformation in the cnidarians (and in the Porifera). What is the mechanistic explanation for this, as some might call it, unpunctuated equilibrium? This "unpuctuated equilibrium" goes under the name of stasis, and has several good explanations. For example, if a species' local environment is unchanged, then all or almost all mutations are harmful, causing natural selection to eliminate variation. The coelacanth is one possibly organism that is unchanged for millions of years in this way. The exact nature of stasis is debated, but there is certainly no lack of hypotheses, as Graham seemingly would have us believe.In 2005 two scientists published a paper titled Adaptive evolution of the human fatty acid synthase gene: Support for the cancer selection and fat utilization hypotheses? To Graham's stated chagrin there is no reference to his work in any form, even though "cancer selection" appears both in title and body of the paper. The authors analyzed how selection has acted on a gene (FAS) involved in both cancer and human brain development, and conclude that the most they can do is speculate that the role played by FAS in one of these two has created a selective pressure for the gene (positive selection), although they can't rule out the various other functions of FAS. In other words, nothing to indicate that cancer selection drives the evolution of complex features. No evidence that Graham's idea has any merit.As a bonus we are told that Graham has these delusions of grandeur. What can you say? Well you can snort and chuckle, I say.Graham goes on to compare himself to Darwin (neither had been educated as a scientist) and Friedrich Wegener of continental drift fame (as a meteorologist not a geologist, Wegener too was an outsider). Thomas Kuhn's classic The Nature of Scientific Revolutions is wheeled out to remind us that people responsible for the "fundamental inventions of a new paradigm have been either very young or very new to the field whose paradigm they change". (The italics are Graham's.) He even compares his method of work to Albert Einstein's.Goodnight.M OCONNELL, J MCINERNEY (2005). Adaptive evolution of the human fatty acid synthase gene: Support for the cancer selection and fat utilization hypotheses? Gene, 360 (2), 151-159 DOI: 10.1016/j.gene.2005.06.020... Read more »

  • January 27, 2009
  • 12:00 AM
  • 1,197 views

Contact with hobbits simplified languages?

by Bjørn Østman in Pleiotropy

Languages simplify only in contact with non-native speakers. Perhaps this happened when humans interacted with hobbits?... Read more »

John McWhorter. (2008) Why does a language undress? Strange cases in Indonesia. Miestamo, Matti, Kaius Sinnemäki and Fred Karlsson (eds.), Language Complexity: Typology, contact, change. 2008. xiv, 356 pp., 167-190.

Tabitha M. Powledge. (2006) What Is the Hobbit?. PLoS Biology, 4(12). DOI: 10.1371/journal.pbio.0040440  

  • March 18, 2009
  • 02:55 PM
  • 1,127 views

Is this a new feathered dinosaur?

by Bjørn Østman in Pleiotropy

Tianyulong confuciusi is a heterodontosaurid dinosaur, which lived in the Early Cretaceous period (144–99 million years ago). The holotype was unearthed in Liaoning Province, China, and is about is about 70 cm long, with a cranium that is 6 cm long.... Read more »

  • November 30, 2008
  • 12:00 AM
  • 1,118 views

Watching multicellularity evolve before our eyes

by Bjørn Østman in Pleiotropy

Chlorella vulgaris is an asexual, unicellular green alga. It has been observed in the laboratory to maintain unicellularity for thousands of generations. Boraas and his collaborators (1998) kept Chlorella for two decades in this way. Then they decided to add a predator, Ochromonas vallescia, also a unicellular organism. It has a flagellum (a tail with which it can swim about), and it eats Chlorella. This is bad news for the Chlorella population, which thus experiences a shift in selective pressure. While it was previously adapted to maximize growth by uptake of nutrients, with Ochromonas around it is suddenly more advantageous to have some sort of defense, even if that should come at a cost of the rate at which it can reproduce.While we could imagine other mechanisms of defense, size is an obvious choice. Very soon (about 10 days) after the introduction of the flagellate predator, Chlorella colonies started to form. These initially consisted of aggregates of tens to hundreds on Chlorella cells, adhering to each other. Their sheer size prevented the predator from eating them, and thus the multicellular Chlorella was fitter than the unicellular ones, and as a result the unicellular Chlorella all but disappeared. Multicellularity had evolved right before the lucky scientists' eyes.Single Chlorella cell (FC), Chlorella colony (CC), and the flagellate predator, Ochromonas (Oc) with its flagellum (Fl).Recall that Chlorella is better able to utilize the nutrients in the environment when they are single cells. Thus, the colonies of tens to hundreds of cells soon disappeared, replaced by colonies of of only eight cells. This seems to be the optimal size for uptake of nutrients and defense against Ochromonas. When Boraas et al. removed the predator from the environment, Chlorella colonies continued to make multicellular offspring. However, with the selection pressure to be large gone, the unicellular Chlorella took over again.The significance of this experiment is that it lends support to the hypothesis that a predator-prey arms race could provide the needed environmental change to enable multicellular organisms to evolve. It also is an outstanding example of observed evolution in the laboratory. It can be argued that the unicellular and multicellular Chlorella are different species, and this is then also an example of speciation observed.Now contrast this Chlorella with the famous E. coli experiment by Blount et al. reported in PNAS this year. In short, after years of culturing E. coli bacteria in the lab, they one day evolved the capacity to metabolize a new nutrient, citrate. Scientists use E. coli's inability to metabolize citrate to distinguish it from other bacteria, so the fact that they suddenly evolved the ability to eat it can also be argued to be an instance of speciation.However, there is a clear difference from Boraas' experiment, namely that Chlorella evolved almost instantly when the selection pressure changed. It thus responded to the change on the basis of standing genetic variation: different genotypes present in the population. There were already some Chlorella cells that were able to adhere to their daughter cells, but it was unfavorable to do so until the appearance of predators. In Blount's experiment it was always favorable to consume citrate. There was plenty of it, and E. coli was deliberately starved on its usual nutrient. Yet they had to wait 30 years to observe E. coli evolving to eat citrate, because the genetic components enabling them to do so had to evolve first. A yet unknown sequence of necessary mutations was required, and once it appeared, E. coli speciated.References:Martin E. Boraas, Dianne B. Seale, Joseph E. Boxhorn (1998). Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity Evolutionary Ecology, 12 (2), 153-164 DOI: 10.1023/A:1006527528063Z. D. Blount, C. Z. Borland, R. E. Lenski (2008). Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli Proceedings of the National Academy of Sciences, 105 (23), 7899-7906 DOI: 10.1073/pnas.0803151105The Chlorella experiment is referenced in chapter 7 of Your Inner Fish by Neil Shubin.... Read more »

  • June 17, 2009
  • 04:21 PM
  • 1,095 views

Homosexuality is not a choice

by Bjørn Østman in Pleiotropy

What are the causes of homosexual behavior in animals? Contrary to what most people probably think, homosexual behavior is not just common in animals, it is catholic.

A new paper in TREE has gotten a lot of press (most papers on sex do, I suspect): Same-sex sexual behavior and evolution, by Bailey and Zuk at UC Riverside.... Read more »

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