Evolutie. Deel XV

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Resurrection of DNA Function In Vivo from an Extinct Genome

There is a burgeoning repository of information available from ancient DNA that can be used to understand how genomes have evolved and to determine the genetic features that defined a particular species. To assess the functional consequences of changes to a genome, a variety of methods are needed to examine extinct DNA function. We isolated a transcriptional enhancer element from the genome of an extinct marsupial, the Tasmanian tiger (Thylacinus cynocephalus or thylacine), obtained from 100 year-old ethanol-fixed tissues from museum collections. We then examined the function of the enhancer in vivo. Using a transgenic approach, it was possible to resurrect DNA function in transgenic mice. The results demonstrate that the thylacine Col2A1 enhancer directed chondrocyte-specific expression in this extinct mammalian species in the same way as its orthologue does in mice. While other studies have examined extinct coding DNA function in vitro, this is the first example of the restoration of extinct non-coding DNA and examination of its function in vivo. Our method using transgenesis can be used to explore the function of regulatory and protein-coding sequences obtained from any extinct species in an in vivo model system, providing important insights into gene evolution and diversity.

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Genetics, Vol. 179, 487-496, May 2008

De Novo Origination of a New Protein-Coding Gene in Saccharomyces cerevisiae
Jing Cai*,{dagger},1, Ruoping Zhao*,1, Huifeng Jiang*,{dagger} and Wen Wang*,2


ABSTRACT Origination of new genes is an important mechanism generating genetic novelties during the evolution of an organism. Processes of creating new genes using preexisting genes as the raw materials are well characterized, such as exon shuffling, gene duplication, retroposition, gene fusion, and fission. However, the process of how a new gene is de novo created from noncoding sequence is largely unknown. On the basis of genome comparison among yeast species, we have identified a new de novo protein-coding gene, BSC4 in Saccharomyces cerevisiae. The BSC4 gene has an open reading frame (ORF) encoding a 132-amino-acid-long peptide, while there is no homologous ORF in all the sequenced genomes of other fungal species, including its closely related species such as S. paradoxus and S. mikatae. The functional protein-coding feature of the BSC4 gene in S. cerevisiae is supported by population genetics, expression, proteomics, and synthetic lethal data. The evidence suggests that BSC4 may be involved in the DNA repair pathway during the stationary phase of S. cerevisiae and contribute to the robustness of S. cerevisiae, when shifted to a nutrient-poor environment. Because the corresponding noncoding sequences in S. paradoxus, S. mikatae, and S. bayanus also transcribe, we propose that a new de novo protein-coding gene may have evolved from a previously expressed noncoding sequence.

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A stem batrachian from the Early Permian of Texas and the origin of frogs and salamanders. Nature, 453, 515-518.

Anderson, J.S. et al. (2008)

The origin of extant amphibians (Lissamphibia: frogs, salamanders and caecilians) is one of the most controversial questions in vertebrate evolution, owing to large morphological and temporal gaps in the fossil record. Current discussions focus on three competing hypotheses: a monophyletic origin within either Temnospondyli or Lepospondyli or a polyphyletic origin with frogs and salamanders arising among temnospondyls and caecilians among the lepospondyls. Recent molecular analyses are also controversial, with estimations for the batrachian (frog–salamander) divergence significantly older than the palaeontological evidence supports. Here we report the discovery of an amphibamid temnospondyl from the Early Permian of Texas that bridges the gap between other Palaeozoic amphibians and the earliest known salientians and caudatans from the Mesozoic. The presence of a mosaic of salientian and caudatan characters in this small fossil makes it a key taxon close to the batrachian (frog and salamander) divergence. Phylogenetic analysis suggests that the batrachian divergence occurred in the Middle Permian, rather than the late Carboniferous as recently estimated using molecular clocks, but the divergence with caecilians corresponds to the deep split between temnospondyls and lepospondyls, which is congruent with the molecular estimates.

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Op donderdag 22 mei 2008 15:40 schreef Triggershot het volgende:
Wat is eigenlijk een evolutionaire voordeel van het overgaan van het bevallen van 'slangjonkies' van eieren naar levend baren?

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Phylogenetic transitions from oviparity to viviparity in reptiles generally have occurred in cold climates, apparently driven by selective advantages accruing from maternal regulation of incubation temperature. But why, then, are viviparous reptiles so successful in tropical climates? Viviparity might enhance fitness in the tropics via the same pathway as in the temperate zone, if pregnant female reptiles in the tropics maintain more stable temperatures than are available in nests (Shine's maternal manipulation hypothesis). Alternatively, viviparity might succeed in the tropics for entirely different reasons than apply in the temperate zone. Our data support the maternal manipulation hypothesis. In a laboratory thermal gradient, pregnant death adders (Acanthophis praelongus) from tropical Australia maintained less variable body temperatures (but similar mean temperatures) than did nonpregnant females. Females kept at a diel range of 25–31°C (as selected by pregnant females) gave birth earlier and produced larger offspring (greater body length and head size) than did females kept at 23–33°C (as selected by nonpregnant snakes). Larger body size enhanced offspring recapture rates (presumably reflecting survival rates) in the field. Thus, even in the tropics, reproducing female reptiles manipulate the thermal regimes experienced by their developing embryos in ways that enhance the fitness of their offspring. This similarity across climatic zones suggests that a single general hypothesis—maternal manipulation of thermal conditions for embryogenesis—may explain the selective advantage of viviparity in tropical as well as cold-climate reptiles.

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What ecological factors might have contributed to the transition to viviparity? The evolution of viviparity has been attributed to selective forces such as environmental factors or biotic traits (e.g. Neill 1964; Packard et al. 1977; Tinkle and Gibbons 1977; Shine and Bull 1979; Shine 1985; Guillette 1993; Qualls and Shine 1998). Since this evolutionary step completely removes the aquatic stage, the obvious responsible agent of this microevolutionary event could be the absence of water in which to lay the larvae, a plausible scenario in some of the islands (Galán 2003). Interestingly, ‘Cíes’ originates for some authors from the Latin ‘siccus’, which means ‘dry’ (González-Alemparte 2003), and today water is scarce in these islands. The lack of available surface water in karstic limestone substrates has also been suggested as the main cause that promotes viviparity in the Cantabric Mountain S. s. bernardezi populations (Garcia-Paris et al. 2003). However, the presence of another amphibian [Lissotriton boscai (Lataste, 1979)] in all water bodies in Ons Island suggests that water limitation was not so drastic at least in Ons. On the other hand, the newts Lissotriton helveticus (Razoumowsky, 1789) and Triturus marmoratus (Latreille, 1800) which are present on the closest coast do not occur in the islands, perhaps due to the absence of favourable habitats, and L. boscai is found only in two islands of the National Park (Ons and Salvora, but not Cíes).

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Dinosaur footprints made 150 million years ago in the bedrock of what is now Yemen are the first to be discovered in the Arabian Peninsula, say scientists.

The two separate trackways were made by a herd of 11 sauropods, and a lone two-legged plant-eating dinosaur belonging to the ornithopod family.

They went unnoticed for so long because they were covered by rubble and debris.

The fossil record in the area is very sparse, with only a handful of dinosaur remains known to science.

A Yemeni journalist stumbled upon the first set of impressions in the village of Madar north of the capital Sana'a.

They were later classified as belonging to an ornithopod, a large, common, two-legged dinosaur that flourished from the Late Triassic Period to the Late Cretaceous Period.

In 2006, a geologist at Sana'a University in Yemen made a further discovery - a set of round and elephant-like footprints from a different dinosaur family, the giant four-legged long-necked sauropods.

Dr Anne Schulp of the Maastricht Museum of Natural History in the Netherlands went out to Yemen to help in the investigation. He said the tracks were "beautifully preserved".

"The nice thing about the sauropod tracks is that we've got a herd of them, 11 individuals all walking in the same direction," Dr Schulp told BBC News.

"It's actually a group consisting of different-sized animals, so we've got old ones and we've got some younger dinosaurs as well, so different age-groups of dinosaurs were living together here."

Only a few dinosaur fossils have been reported so far from the Arabian Peninsula, including isolated bones from Oman and possible fragments of a long-necked dinosaur from Yemen.

"It's the first time we've found dinosaur trackways in the Arab Peninsula so it really is a first," said Dr Schulp.

"It's a bit of data from a place that we really don't know much about yet. There is a lot of potential for more discoveries."

Palaeontologist Dr Paul Barrett of London's Natural History Museum said the findings, published in the journal PLoS One, considerably expand our knowledge of Middle Eastern dinosaurs.

"Dinosaur material is exceptionally rare in this part of the world, and is represented by only a handful of fragmentary fossils," he said.

"As a result, we know virtually nothing about the animals that once roamed this area. This discovery shows that several different kinds of dinosaur were abundant in the region and starts to fill a large gap in our knowledge of what was going on in the Middle East during the age of the dinosaurs."

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Session 1: Archaean Chemistry and Earliest Fossils

* The RNA World and the Molecular Origins of Life Gerald F. Joyce, The Scripps Research Institute

* The Origins of Cellular Life Jack W. Szostak, Harvard Medical School

* Can the Distribution of Protein Domains Shed Light on the Tree of Life Russell F. Doolittle, University of California, San Diego

* The Earliest Life on Earth Roger Buick, University of Washington

* Proterozoic Life and Environments Andrew H. Knoll, Harvard University

Session 2: Cells, Cellular Evolution and Protein History

* The Tree of Life and Major Transitions in Cell Evolution Thomas Cavalier-Smith, University of Oxford

* The Origin of Eukaryotes Eugene V. Koonin, National Center for Biotechnology Information, National Institutes of Health

* Barking up the Wrong Tree: The Dangers of Reification in Molecular Phylogenetics and Systematics W. Ford Doolittle, Dalhousie University

* RNA Interference May Provide a Window on the RNA-to-DNA World Transition Phillip A. Sharp, Massachusetts Institute of Technology

Evening Lecture, 6 – 7 p.m.

Feeding and Gloating for More: The Challenge of the New Creationism Jerry A. Coyne, The University of Chicago

Session 3: Development of Eukaryotic Genetic Capacity and Multicellularity

* The Deep Evolutionary History of Eukaryotes Andrew Roger, Dalhousie University

* Demonstrating the Sufficiency of Microevolutionary Processes David Penny, Massey University

* Genes and Development: A Comparison of Human and Amphioxus Genomes Peter W.H. Holland, University of Oxford

* Cnidaria and the Evolution of the Bilaterian Body Plans: Insights from an Outgroup Ulrich Technau, University of Vienna

Session 4: Human Evolution through the Lens of DNA Sequences

* Evolution of Human Populations L. Luca Cavalli-Sforza, Stanford University School of Medicine

* Accelerated Evolution in the Human Genome Katherine S. Pollard, University of California, Davis

* Probing Human Brain Evolution at the Genetic Level Bruce T. Lahn, The University of Chicago

* A Neanderthal Perspective on Human Origins Fairfield Osborn Memorial Lecture , Svante Pääbo, Max Planck Institute for Evolutionary Anthropology

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One of the most important experiments in evolution is going on right now in a laboratory in Michigan State University. A dozen flasks full of E. coli are sloshing around on a gently rocking table. The bacteria in those flasks has been evolving since 1988--for over 44,000 generations. And because they've been so carefully observed all that time, they've revealed some important lessons about how evolution works.

The experiment was launched by MSU biologist Richard Lenski. I wrote about Lenski's work last year in the New York Times, and in more detail my new book Microcosm. Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.

Based on what scientists already knew about evolution, Lenski expected that the bacteria would experience natural selection in their new environment. In each generation, some of the microbes would mutate. Most of the mutations would be harmful, killing the bacteria or making them grow more slowly. Others would be beneficial allowing them to breed faster in their new environment. They would gradually dominate the population, only to be replaced when a new mutation arose to produce an even fitter sort of microbe.

Lenski used a simple but elegant method to find out if this would happen. He froze some of the original bacteria in each line, and then froze bacteria every 500 generations. Whenever he was so inclined, he could go back into this fossil record and thaw out some bacteria, bringing them back to life. By putting the newest bacteria in his lines in a flask along with their ancestors, for example, he could compare how well the bacteria had adapted to the environment he had created.

Over the generations, in fits and starts, the bacteria did indeed evolve into faster breeders. The bacteria in the flasks today breed 75% faster on average than their original ancestor. Lenski and his colleagues have pinpointed some of the genes that have evolved along the way; in some cases, for example, the same gene has changed in almost every line, but it has mutated in a different spot in each case. Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they've gotten worse at feeding on some other kinds of sugars.

Last year Lenski was elected to the National Academy of Sciences. This week he is publishing an inaugural paper in the Proceedings of the National Academy of Sciences with his student Zachary Blount and postdoc Christina Borland. Lenski told me about the discovery behind the paper when I first met him a few years ago. He was clearly excited, but he wasn't ready to go public. There were still a lot of tests to run to understand exactly what had happened to the bacteria.

Now they're sure. Out of the blue, their bacteria had abandoned Lenski's their glucose-only diet and had evolved a new way to eat.

After 33,127 generations Lenski and his students noticed something strange in one of the colonies. The flask started to turn cloudy. This happens sometimes when contaminating bacteria slip into a flask and start feeding on a compound in the broth known as citrate. Citrate is made up of carbon, hydrogen, and oxygen; it's essentially the same as the citric acid that makes lemons tart. Our own cells produce citrate in the long chain of chemical reactions that lets us draw energy from food. Many species of bacteria can eat citrate, but in an oxygen-rich environment like Lenski's lab, E. coli can't. The problem is that the bacteria can't pull the molecule in through their membranes. In fact, their failure has long been one of the defining hallmarks of E. coli as a species.

If citrate-eating bacteria invade the flasks, however, they can feast on the abundant citrate, and their exploding population turns the flask cloudy. This has only happened rarely in Lenski's experiment, and when it does, he and his colleagues throw out the flask and start the line again from its most recently frozen ancestors.

But in one remarkable case, however, they discovered that a flask had turned cloudy without any contamination. It was E. coli chowing down on the citrate. The researchers found that when they put the bacteria in pure citrate, the microbes could thrive on it as their sole source of carbon.

In nature, there have been a few reports of E. coli that can feed on citrate. But these oddballs all acquired a ring of DNA called a plasmid from some other species of bacteria. Lenski selected a strain of E. coli for his experiments that doesn't have any plasmids, there were no other bacteria in the experiment, and the evolved bacteria remain plasmid-free. So the only explanation was that this one line of E. coli had evolved the ability to eat citrate on its own.

Blount took on the job of figuring out what happened. He first tried to figure out when it happened. He went back through the ancestral stocks to see if they included any citrate-eaters. For the first 31,000 generations, he could find none. Then, in generation 31,500, they made up 0.5% of the population. Their population rose to 19% in the next 1000 generations, but then they nearly vanished at generation 33,000. But in the next 120 generations or so, the citrate-eaters went berserk, coming to dominate the population.

This rise and fall and rise suggests that the evolution of citrate-eating was not a one-mutation affair. The first mutation (or mutations) allowed the bacteria to eat citrate, but they were outcompeted by some glucose-eating mutants that still had the upper hand. Only after they mutated further did their citrate-eating become a recipe for success.

The scientists wondered if other lines of E. coli carried some of these invisible populations of weak citrate-eaters. They didn't. This was quite remarkable. As I said earlier, Lenski's research has shown that in many ways, evolution is repeatable. The 12 lines tend to evolve in the same direction. (They even tend to get plump, for reasons yet to be understood.) Often these parallel changes are the result of changes to the same genes. And yet when it comes to citrate-eating, evolution seems to have produced a fluke.

To gauge the flukiness of the citrate-eaters, Blount and Lenski replayed evolution. They grew new populations from 12 time points in the 33,000-generations of pre-citrate-eating bacteria. They let the bacteria evolve for thousands of generations, monitoring them for any signs of citrate-eating. They then transferred the bacteria to Petri dishes with nothing but citrate to eat. All told, they tested 40 trillion cells. Here's a movie of what that looks like...

ut of that staggering hoard of bacteria, only a handful of citrate-eating mutants arose. None of the original ancestors or early predecessors gave rise to citrate-eaters; only later stages in the line could--mostly from 27,000 generations or beyond. Still, even among these later E. coli, the odds of evolving into a citrate-eater was staggeringly low, on the order of one-in-a-trillion.

Now the scientists must determine the precise genetic steps these bacteria took to evolve from glucose-eaters to citrate-eaters. In order to eat a particular molecule, E. coli needs a special channel in its membranes through which to draw it. It's possible, for example, that a channel dedicated to some other molecule mutated into a form that could also take in citrate. Later mutations could have fine-tuned it so that it could suck in citrate quickly.

If E. coli is defined as a species that can't eat citrate, does that mean that Lenski's team has witnessed the origin of a new species? The question is actually murkier than it seems, because the traditional concept of species doesn't fit bacteria very comfortably. (For the details, check out my new article on Scientific American, "What is a Species?") In nature, E. coli swaps lots of genes with other species. In just the past 15 years or so, for example, one disease-causing strain of E. coli acquired hundreds of genes not found in closely related E. coli strains. (See my recent article in Slate.) Another hallmark of E. coli is its ability to break down lactose, the sugar in milk. But several strains have lost the ability to break it down. (In fact, these strains were originally given a different name--Shigella--until scientists realized that they were just weird strains of E. coli.)

Nevertheless, Lenski and his colleagues have witnessed a significant change. And their new paper makes clear that just because the odds of such a significant change are incredibly rare doesn't mean that it can't happen. Natural selection, in fact, ensures that sometimes it does. And, finally, it demonstrates that after twenty years, Lenski's invisible dynasty still has some surprises in store.

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Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli
Zachary D. Blount, Christina Z. Borland, and Richard E. Lenski

The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit+) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. The long-delayed and unique evolution of this function might indicate the involvement of some extremely rare mutation. Alternately, it may involve an ordinary mutation, but one whose physical occurrence or phenotypic expression is contingent on prior mutations in that population. We tested these hypotheses in experiments that "replayed" evolution from different points in that population's history. We observed no Cit+ mutants among 8.4 x 10¹² ancestral cells, nor among 9 x 10¹² cells from 60 clones sampled in the first 15,000 generations. However, we observed a significantly greater tendency for later clones to evolve Cit+, indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit+ but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection.

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Op woensdag 11 juni 2008 12:24 schreef ATuin-hek het volgende:
Voor de matlabbers onder ons Ik ben atm bezig met een genetisch algoritme om een MRI bias field correctie te berekenen voor FLAIR scans. Is best leuk om mee te spelen Geeft een aardig gevoel over hoe krachtig een evolutionaire aanpak kan zijn.
Als het goed is wordt mijn werk onderdeel van een publicatie. Zal kijken of ik die tegen die tijd hier kan linken

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Evolution’s recipe for making a brain more complex has long seemed simple enough. Just increase the number of nerve cells, or neurons, and the interconnections between them. A human brain, for instance, is three times the volume of a chimpanzee’s.

A whole new dimension of evolutionary complexity has now emerged from a cross-species study led by Dr. Seth Grant at the Sanger Institute in England.

Dr. Grant looked at the interconnections between neurons, known as synapses, which until now have been regarded as a standard feature of neurons.

But in fact the synapses get considerably more complex going up the evolutionary scale, Dr. Grant and colleagues reported online Sunday in Nature Neuroscience. In worms and flies, the synapses mediate simple forms of learning, but in higher animals they are built from a much richer array of protein components and conduct complex learning and pattern recognition, Dr. Grant said.

The finding may open a new window into how the brain operates. “One of the biggest questions in neuroscience is to answer what are the design principles by which the human brain is constructed, and this is one of those principles,” Dr. Grant said.

If the synapses are thought of as the chips in a computer, then brainpower is shaped by the sophistication of each chip, as well as by their numbers. “From the evolutionary perspective, the big brains of vertebrates not only have more synapses and neurons, but each of these synapses is more powerful — vertebrates have big Internets with big computers and invertebrates have small Internets with small computers,” Dr. Grant said.

He included yeast cells in his cross-species survey and found that they contain many proteins equivalent to those in human synapses, even though yeast is a single-celled microbe with no nervous system. The yeast proteins, used for sensing changes in the environment, suggest that the origin of the nervous system, or at least of synapses, began in this way.

The computing capabilities of the human brain may lie not so much in its neuronal network as in the complex calculations that its synapses perform, Dr. Grant said. Vertebrate synapses have about 1,000 different proteins, assembled into 13 molecular machines, one of which is built from 183 different proteins.

These synapses are not standard throughout the brain, Dr. Grant’s group has found; each region uses different combinations of the 1,000 proteins to fashion its own custom-made synapses.

Each synapse can presumably make sophisticated calculations based on messages reaching it from other neurons. The human brain has about 100 billion neurons, interconnected at 100 trillion synapses.

The roots of several mental disorders lie in defects in the synaptic proteins, more than 50 of which have been linked to diseases like schizophrenia, Dr. Grant said.

Dr. Edward Ziff, a synapse expert at New York University, said Dr. Grant’s work was the first in which synapses had been analyzed from a cross-species perspective. “I would say this work is unique,” he said. “Grant’s been a leader in making this type of analysis and he deserves a lot of credit for it, although a certain amount of guesswork is involved.”

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Op donderdag 12 juni 2008 11:45 schreef ATuin-hek het volgende:

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Zoiets ja De sterkte van het signaal dat van een bepaalde voxel komt hangt oa af van de magneetsterkte op die positie. Ideaal gezien is dit uniform, maar in de praktijk helaas niet.
FLAIR scans hebben gelukkig het voordeel dat er maar 1 piek zit in het histogram. Mijn algoritme zoekt een benadering van het bias field zodat deze piek zo scherp mogelijk wordt De mate van scherpte is dus de mate van fitness.

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Op donderdag 12 juni 2008 13:44 schreef ATuin-hek het volgende:

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Ik ben idd ook met zoiets bezig Doe samen met de begeleiders een poging om MS laesies automatisch te segmenteren. Komt ook registratie etc. bij kijken.

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Natural Selection Shapes Genome-Wide Patterns of Copy-Number Polymorphism in Drosophila melanogaster
J. J. Emerson, Margarida Cardoso-Moreira, Justin O. Borevitz, Manyuan Long


The role that natural selection plays in governing the locations and early evolution of copy-number mutations remains largely unexplored. We used high-density full-genome tiling arrays to create a fine-scale genomic map of copy-number polymorphisms (CNPs) in Drosophila melanogaster. We inferred a total of 2658 independent CNPs, 56% of which overlap genes. These include CNPs that are likely to be under positive selection, most notably high-frequency duplications encompassing toxin-response genes. The locations and frequencies of CNPs are strongly shaped by purifying selection, with deletions under stronger purifying selection than duplications. Among duplications, those overlapping exons or introns, as well as those falling on the X chromosome, seem to be subject to stronger purifying selection.

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Op vrijdag 20 juni 2008 18:12 schreef Papierversnipperaar het volgende:

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Ik snap veel, maar dit is me iets te technisch. Kan je dit vertalen in Jip en Janneketaal?

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Differences in the numbers of copies of large DNA segments are an abundant source of genetic variation in humans (1, 2), mice (3), and flies (4). Because CNPs can create new genes, change gene dosage, reshape gene structures, and/or modify the elements that regulate gene expression, understanding their evolution is at the very heart of understanding how such structural changes in the genome contribute to the phenotypic evolution of organisms.

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The all-female worker caste of the honey bee (Apis mellifera) is effectively barren in that workers refrain from laying eggs in the presence of a fecund queen. The mechanism by which workers switch off their ovaries in queenright colonies is pheromonally cued, but there is genetically-based variation among individuals: some workers have high thresholds for ovary activation, while for others the response threshold is lower. Genetic variation for threshold response by workers to ovary-suppressing cues is most evident in "anarchist" colonies in which mutant patrilines have a proportion of workers that activate their ovaries and lay eggs, despite the presence of a queen. In this study we use a selected anarchist line to create a backcross queenright colony that segregated for high and low levels of ovary activation. We used 191 informative microsatellite loci, covering all 16 linkage groups to identify QTLs for ovary activation and test the hypothesis that anarchy is recessively inherited. We reject this hypothesis, but identify four QTLs that together explain approximately 25% of the phenotypic variance for ovary activation in our mapping population. They provide the first molecular evidence for the existence of quantitative loci that influence selfish cheating behavior in a social animal.

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Op dinsdag 24 juni 2008 23:39 schreef Triggershot het volgende:
Waarom ziet de mens eigenlijk in kleur?

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Ventastega curonica and the origin of tetrapod morphology
Per E. Ahlberg, Jennifer A. Clack, Ervi macrns Luks caronevic carons, Henning Blom & Ivars Zupincedils caron

The gap in our understanding of the evolutionary transition from fish to tetrapod is beginning to close thanks to the discovery of new intermediate forms such as Tiktaalik roseae. Here we narrow it further by presenting the skull, exceptionally preserved braincase, shoulder girdle and partial pelvis of Ventastega curonica from the Late Devonian of Latvia, a transitional intermediate form between the 'elpistostegids' Panderichthys and Tiktaalik and the Devonian tetrapods (limbed vertebrates) Acanthostega and Ichthyostega. Ventastega is the most primitive Devonian tetrapod represented by extensive remains, and casts light on a part of the phylogeny otherwise only represented by fragmentary taxa: it illuminates the origin of principal tetrapod structures and the extent of morphological diversity among the transitional forms.

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Op donderdag 26 juni 2008 11:53 schreef Terecht het volgende:
Hoi, ik heb een vraagje.

Ik ben de laatste tijd wat aan het lezen over evolutie, en nu vraag ik me af of Darwinisme nou wel of niet falsifieerbaar is. Ik heb deze FAQ van Talkorigins gelezen, maar ik ben er nog niet helemaal uit. Misschien dat het nog even moet bezinken, maar klopt het dat het wel of niet falsifieerbaar zijn van Darwinisme in weze staat of valt bij welke definitie van falsifieerbaarheid je aanhangt?

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Op donderdag 26 juni 2008 12:19 schreef Terecht het volgende:

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Wel, ik sprak laatst iemand die zei dat de evolutietheorie niet falsifieerbaar is. Toen ben ik eens op zoek gegaan wat daar nou van waar is, maar van de Talkorigins FAQ ben ik nog niet echt veel wijzer geworden . Als ik het goed begrepen heb, ligt het vooral aan welke criteria je aan het begrip falsifieerbaarheid wilt toekennen of evolutionaire biologie (Darwinian evolution?) falsifieerbaar is of niet.. Klopt dit, of zit ik er gruwelijk naast? Misschien is de vraagstelling wel iets te algemeen, maar zo bekend ben ik niet met de wetenschap achter evolutie .

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Op donderdag 26 juni 2008 09:55 schreef Monolith het volgende:

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Nature