Contrary to predictions, males of high genetic quality are not very successful when it comes to fertilizing eggs.

SOURCE

Contrary to predictions, males of high genetic quality are not very successful when it comes to fertilizing eggs. A new study on seed beetles by Swedish and Danish scientists Göran Arnqvist and Trine Bilde shows that when a female mates with several males, the males of low genetic quality are the most successful in fertilizing eggs. The study is published in this week's issue of Science.

In almost all animals, females mate with several different males, despite the fact that a single mating is often sufficient to fertilize her eggs. Multiple mating also carries costs to females, such as the risk of catching sexually transmitted diseases.
One commonly held belief is that this behaviour may allow females to choose the sperm of the male with highest genetic quality to fertilize her eggs. Professor Göran Arnqvist from the Department of Ecology and Evolution, Uppsala University and associate professor Trine Bilde from the Department of Biological Sciences, University of Aarhus, have tested this possibility directly for the first time and shown that it is not true.
Their study on seed beetles shows that, contrary to predictions, males of low genetic quality are more successful in fertilizing eggs. Males who gained the highest share of paternity were actually males with low genetic quality. These males also fathered offspring that did less well.
"The results support the suggestion that genes that are good for males may often be bad for their mates. Therefore, in beetles at least, multiple mating does not award females with genetic benefits," says Göran Arnqvist.
Source: Uppsala University (news : web)

Geography And History Shape Genetic Differences In Humans

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ScienceDaily (June 5, 2009) — New research indicates that natural selection may shape the human genome much more slowly than previously thought. Other factors -- the movements of humans within and among continents, the expansions and contractions of populations, and the vagaries of genetic chance – have heavily influenced the distribution of genetic variations in populations around the world.

The study, conducted by a team from the Howard Hughes Medical Institute, the University of Chicago, the University of California and Stanford University, is published June 5 in the open-access journal PLoS Genetics.
In recent years, geneticists have identified a handful of genes that have helped human populations adapt to new environments within just a few thousand years—a strikingly short timescale in evolutionary terms. However, the team found that for most genes, it can take at least 50,000-100,000 years for natural selection to spread favorable traits through a human population. According to their analysis, gene variants tend to be distributed throughout the world in patterns that reflect ancient population movements and other aspects of population history.
"We don't think that selection has been strong enough to completely fine-tune the adaptation of individual human populations to their local environments," says co-author Jonathan Pritchard. "In addition to selection, demographic history -- how populations have moved around -- has exerted a strong effect on the distribution of variants."
To determine whether the frequency of a particular variant resulted from natural selection, Pritchard and his colleagues compared the distribution of variants in parts of the genome that affect the structure and regulation of proteins to the distribution of variants in parts of the genome that do not affect proteins. Since these neutral parts of the genome are less likely to be affected by natural selection, they reasoned that studying variants in these regions should reflect the demographic history of populations.
The researchers found that many previously identified genetic signals of selection may have been created by historical and demographic factors rather than by selection. When the team compared closely related populations they found few large genetic differences. If the individual populations' environments were exerting strong selective pressure, such differences should have been apparent.
Selection may still be occurring in many regions of the genome, says Pritchard. But if so, it is exerting a moderate effect on many genes that together influence a biological characteristic. "We don't know enough yet about the genetics of most human traits to be able to pick out all of the relevant variation," says Pritchard. "As functional studies go forward, people will start figuring out the phenotypes that are associated with selective signals," says lead author Graham Coop. "That will be very important, because then we can figure out what selection pressures underlie these episodes of natural selection."
But even with further research, much will remain unknown about the processes that have resulted in human traits. In particular, Pritchard and Coop urge great caution in trying to link selection with complex characteristics like intelligence. "We're in the infancy of trying to understand what signals of selection are telling us," says Coop, "so it's a very long jump to attribute cultural features and group characteristics to selection."
Journal reference:
Coop G, Pickrell JK, Novembre J, Kudaravalli S, Li J, et al. The Role of Geography in Human Adaptation. PLoS Genetics, 2009; 5 (6): e1000500 DOI: 10.1371/journal.pgen.1000500
Adapted from materials provided by Public Library of Science, via EurekAlert!, a service of AAAS.

Chemists see first building blocks to life on Earth

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British scientists said on Wednesday that they had figured out key steps in the process by which life on Earth may have emerged from a seething soup of simple chemicals.

Genetic information in living organisms today is held in deoxyribonucleic acid (DNA), the famous "double helix" molecule of sugar, phosphate and a base.
But DNA is too sophisticated to have popped up in an instant, and one avenue of thought says its single-stranded cousin, ribonucleic acid, or RNA, came first.
RNA plays a key role in making proteins and, in viruses, is used to store genetic code.
It is chemically similar to DNA but is simpler and tougher in structure, and thus looks like a good candidate for Earth's first information-coding nucleic acid.
But for all its allure, the "RNA first" theory has run into practical problems.
Its three ingredients -- the base, ribose sugar and phosphate -- must have formed separately and then combined to form the molecule, according to conventional thinking.
Critics, though, say that RNA, while somewhat simpler than DNA, is still a complex molecule and could not have been assembled spontaneously.
These doubters have been comforted by the failure to find any feasible chain of chemical events to explain how the three components all came together.
But a paper published in the British journal Nature by University of Manchester chemists puts forward a different explanation.
The team, led by Professor John Sutherland, venture that an RNA-like synthesis took place through a series of chemical reactions and an important intermediate substance.
Their lab model uses starting materials and environmental conditions that are believed to have been around in early Earth and are also used in the standard "RNA first" scenario.
Their theory starts with a simple sugar called glycolaldehyde, which reacts with cyanmide (a compound of cyanide and ammonia) and phosphate to produce an intermediate compound called 2-aminooxazole.
Gentle warming from the Sun and cooling at night help purify the 2-aminooxazole, turning it into a plentiful precursor which contributes the sugar and base portions of the new ribonucleotide molecule.
The presence of phosphate and ultraviolet light from the Sun complete the synthesis.
In a commentary also published by Nature, US molecular biologist Jack Szostak hailed the research as an elegant explanation as to why the sugar and base would not have to form separately before forming the new molecule.
"It will stand for years as one of the great advances in prebiotic chemistry," the term for the study of the chemical processes that led to life on Earth, he enthused.
Opinions vary as to when the first organisms appeared on Earth.
One estimate, based on fossilised mats of bacteria found in Australia, is that this happened around 3.8 billion years ago, around 700 million years after the planet was formed.
(c) 2009 AFP

Beyond A 'Speed Limit' On Mutations, Species Risk Extinction

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http://www.sciencedaily.com/releases/2007/10/071001172753.htm

Science Daily — Harvard University scientists have identified a virtual "speed limit" on the rate of molecular evolution in organisms, and the magic number appears to be 6 mutations per genome per generation -- a level beyond which species run the strong risk of extinction as their genomes lose stability.
By modeling the stability of proteins required for an organism's survival, Eugene Shakhnovich and his colleagues have discovered this essential thermodynamic limit on a species's rate of evolution. Their discovery, published recently in the Proceedings of the National Academy of Sciences, draws a crucial connection between the physical properties of genetic material and the survival fitness of an entire organism.
"While mathematical genetics research has brought about some remarkable discoveries over the years, these approaches always failed to connect the dots between the reproductive fitness of organisms and the molecular properties of the proteins encoded by their genomes," says Shakhnovich, professor of chemistry and chemical biology in Harvard's Faculty of Arts and Sciences. "We've made an important step toward finally bridging the gap between macroscopic and microscopic biology."
According to Shakhnovich, crucial aspects of an organism's evolutionary fitness can be directly inferred by inspecting its DNA sequences and analyzing how the proteins encoded by those sequences fold. DNA sequences encode the order of amino acids in a protein, and amino acids act as the protein's basic building blocks by arranging themselves into a structure that allows the protein to perform its biological function.
The research was inspired in part by the longstanding recognition that knocking out essential genes, making them inactive, produces a lethal phenotype, or a physiologically unviable organism.
"From there, we made the simple assumption that in order for an organism to be viable, all of its essential genes -- those that support basic cell operations -- have to encode at least minimally stable proteins," says Shakhnovich. "What occurs over the long process of evolution is that random mutations can either encode slightly more or less stable proteins."
If enough mutations push an essential protein towards an unstable, non-functional structure, the organism will die. Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material.
The existence of a mutation limit for viruses helps explain how the immune system can perform its function. Because viral replication and survival can only occur at a limited rate, the body has a window of time to develop antibodies against infectious agents. Furthermore, if the mutation rate is high, the size of the genome in question must be small to stay within the bounds of the speed limit -- thus organisms that tend to mutate quickly are those with concise genomes, such as viruses and bacteria.
The Shakhnovich speed limit also offers an explanation for observed differences in genome sizes between organisms with genome error correction -- such as bacteria, mammals, birds, and reptiles -- and those without, such as RNA viruses: In more complex organisms, cells have evolved correction systems to detect and fix errors in DNA replication. These systems drastically reduce the number of mutations per replication, increasing the mutational stability of the genome and allowing more intricate and delicate biological systems to develop without the risk of interruptive mutations.
"It's an interesting corollary because it suggests that there is a fundamental tradeoff between evolutionary security and adaptive flexibility: Larger, more complex organisms have to have error correction to protect organismic viability, but this means the rate of evolution slows down significantly," Shakhnovich says. "As organisms become more complex, they have more to lose and can't be as radically experimental with their genomes as some viruses and bacteria."
Co-authors on the paper are Konstantin B. Zeldovich of the Department of Chemistry and Chemical Biology and Peiqiu Chen of the departments of Physics and of Chemical and Chemical Biology in Harvard's Faculty of Arts and Sciences. Their work is funded by the National Institutes of Health.
Note: This story has been adapted from material provided by Harvard University.

Fausto Intilla
www.oloscience.com

New Method Can Reveal Ancestry Of All Genes Across Many Different Genomes

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http://www.sciencedaily.com/releases/2007/09/070911155206.htm

Science Daily — The wheels of evolution turn on genetic innovation -- new genes with new functions appear, allowing organisms to grow and adapt in new ways. But deciphering the history of how and when various genes appeared, for any organism, has been a difficult and largely intractable task.

Now a team led by scientists at the Broad Institute of MIT and Harvard has broken new ground by developing a method, described in the September 6 advance online edition of Nature, that can reveal the ancestry of all genes across many different genomes. First applied to 17 species of fungi, the approach has unearthed some surprising clues about why new genes pop up in the first place and the biological nips and tucks that bolster their survival.
"Having the ability to trace the history of genes on a genomic scale opens the doors to a vast array of interesting and largely unexplored scientific questions," said senior author Aviv Regev, an assistant professor of biology at MIT and a core member of the Broad Institute. Although the principles laid out in the study pertain to fungi, they could have relevance to a variety of other species as well.
It has been recognized for decades that new genes first arise as carbon copies of existing genes. It is thought that this replication allows one of the gene copies to persist normally, while giving the other the freedom to acquire novel biological functions. Though the importance of this so-called gene duplication process is well appreciated -- it is the grist for the mill of evolutionary change -- the actual mechanics have remained murky, in part because scientists have lacked the tools to study it systematically.
Driven by the recent explosion of whole genome sequence data, the authors of the new study were able to assemble a natural history of more than 100,000 genes belonging to a group of fungi known as the Ascomycota. From this, the researchers gained a detailed view of gene duplication across the genomes of 17 different species of fungi, including the laboratory model Saccharomyces cerevisiae, commonly known as baker's yeast.
The basis for the work comes from a new method termed "SYNERGY", which first author Ilan Wapinski and his coworkers developed to help them reconstruct the ancestry of each fungal gene. By tracing a gene's lineage through various species, the method helps determine in which species the gene first arose, and if -- and in what species -- it became duplicated or even lost altogether. SYNERGY draws its strength from the use of multiple types of data, including the evolutionary or "phylogenetic" tree that depicts how species are related to each other, and the DNA sequences and relative positions of genes along the genome.
Perhaps most importantly, the method does not tackle the problem of gene origins in one fell swoop, as has typically been done, but rather breaks it into discrete, more manageable bits. Instead of treating all species at once, SYNERGY first focuses on a pair of the most recently evolved species -- those at the outer branches of the tree -- and works, two-by-two, toward the more ancestral species that comprise the roots.
From this analysis, Regev and her colleagues were able to identify a set of core principles that govern gene duplication in fungi. The findings begin to paint a picture of how new genes are groomed over hundreds of millions of years of evolution.
The study was supported by grants from the Burroughs Wellcome Fund and the National Institute of General Medical Sciences.
Note: This story has been adapted from a news release issued by Massachusetts Institute Of Technology.

Fausto intilla

www.oloscience.com

Parasitic Battles Can Involve Gene Transfer That Aids Evolution

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http://www.sciencedaily.com/releases/2007/09/070905134534.htm

Science Daily — Scientists at MIT's Department of Civil and Environmental Engineering and the Technion Israel Institute of Technology have for the first time recorded the entire genomic expression of both a host bacterium and an infecting virus over the eight-hour course of infection.

The results of this research likely will encourage scientists in several fields to rethink their approach to the study of host-virus systems, which are believed to play a key evolutionary role by facilitating the transfer of genes between species.
Professors Debbie Lindell of the Technion and Sallie Chisholm of MIT and co-authors report in the Sept. 6 issue of Nature that their study of a system involving the marine bacteria, Prochlorococcus, leads them to speculate that viral infection may play a role in shaping the genetic repertoire of families of bacteria, even though individual infected bacteria die.
This could indicate that the meeting between a marine bacterial host and its virus may not be just a battle between two individuals, but an evolutionarily significant exchange that helps both species become more fit for life in the ocean environment.
"The current status of host-virus relations has been influenced by a rich history of interactions," said Lindell. "While we can't definitively pin down the sequence of past co-evolutionary events, our findings suggest a novel means through which the exchange of beneficial genes between host and virus have been triggered."
And, because the pattern of genomic expression in this host-virus system differed significantly from that in the more commonly studied system of intestinal bacteria such as E. coli and a virus called T7, the research will likely lead to increased appreciation for the need to study diverse types of marine bacteria, rather than relying on a single system as a broad model.
"We hope this work will encourage scientists to explore a wide range of host-pathogen systems and thus lead to a significant broadening of our understanding of the diversity of the host-pathogen interactions existing in nature," said Chisholm, one of the discoverers of Prochlo-rococcus in 1985. "More importantly, these studies will help us understand the role these interactions play in shaping microbial ecosystems."
Researchers have only in the past few decades begun discovering and studying ecologically relevant ocean bacteria, such as Prochlorococcus, which play a very important role in our lives. These single-celled photosynthetic bacteria use light energy to produce oxygen and organic carbon --supplying a significant portion of the oxygen we breathe--and forming the basis for the ocean food chain.
In previously studied host-virus systems, a virus hijacks the bacterial host cell and shuts down genome expression immediately, preventing the bacterium from conducting its own metabolic processes. The attacking virus redirects expression to its own genome and activates the genes beneficial for its activity, which is to replicate itself quickly at the cost of the host.
But uncharacteristically, in the system of Prochlorococcus and virus P-SSP7, an unprecedented 41 of the bacteria's 1,717 genes were upregulated. That is, the researchers detected increased quantities of the messenger RNA encoded by these genes in the cell during the infection process. The upregulation of so many host genes during infection is a phenomenon unseen before in the world of bacteriology.
Moreover, many of the host genes upregulated during infection are among those that are found in genomic islands in the host, variable regions that appear to be hot-spots for genetic exchange between bacterial hosts and viruses. In this case, some of the genes that have been transferred back and forth encode for proteins that affect the bacteria's ability to adapt to changes in environmental factors, such as nutrient deprivation and light stress. The scientists hypothesize that modifications made to the bacterial genes when they were in the virus led to new versions of the proteins that may provide the bacteria with an increased ability to withstand environmental changes. It is also possible that multiple copies of a gene provide some benefit.
Another unusual occurrence is that the viral genome contains genes transferred from bacterial hosts that encode energy-producing proteins, including photosynthesis genes that cyanobacteria need for metabolism and DNA replication. Although these genes are positioned far apart in the viral genome, they are transcribed at the same time during infection rather than in the usual left-to-right order. This leads the researchers to surmise that the virus is trying to keep its host alive longer so that the host continues to provide the energy needed for the virus's own DNA replication.
Lindell and Chisholm believe the most plausible scenario to explain the gene upregulation and gene trading is that the bacterium activates certain genes in response to infection as a means of self-protection. The virus has "learned" to use those genes to its own advantage and so incorporates them into its own genome. Later, when infecting another bacterium, the virus upregulates those genes itself to facilitate its own reproduction within the host bacterium. When a bacterium survives an infection, those viral modified genes are incorporated back into the bacterial DNA in genome islands, making that bacterium and its descendants more likely to survive in the harsh ocean environment.
"These viral parasites cooperate with their hosts during infection, providing proteins that probably function within host metabolic pathways, to squeeze every bit of energy out them before killing them off," said Lindell. "Yet on evolutionary scales, such host-pathogen interactions are influencing the evolution of gene content in both host and virus, which in turn is likely impacting their ability to colonize new niches."
Next steps in the research are to see if the host-like genes in the virus really do confer a fitness advantage to the virus and then to the host bacterium when transferred back.
Funding for this research came from the Department of Energy's GTL Program, the Gordon and Betty Moore Foundation, and the National Science Foundation.
Lindell performed the research as a postdoctoral associate in Chisholm's lab before joining the Technion faculty in the Department of Biology in October 2006. It builds on previous work in Chisholm's lab at MIT, including research by Lindell and co-author Matthew Sullivan, who in 2004 noted the presence of host genes in the viruses and their transfer back to the host, and by Maureen Coleman, who in 2006 found genomic islands in the host that had most likely come from viruses.
Other authors are MIT graduate students Gregory Kettler and Coleman; MIT postdoctoral associate Sullivan; Jacob Jaffe of the Broad Institute; Matthias Futschik and Ilka Axmann of Humboldt University; Trent Rector, Robert Steen and George Church of Harvard Medical School; and Wolfgang Hess of the University of Freiburg.
Note: This story has been adapted from a news release issued by Massachusetts Institute of Technology.

Fausto Intilla

www.oloscience.com

New Species May Form WIth A Little Help From Immune System

Source:

http://www.sciencedaily.com/releases/2007/09/070905103023.htm

Science Daily — Plant geneticists and animal breeders alike know the problem: single individuals or entire broods will not thrive, some die early, or remain, even if they survive, the runts of the litter and thus not useful for continued breeding programs. What is annoying for the breeder, fascinates geneticists and molecular biologists. The unfit offspring are an example that genetic material cannot always be combined at will.

Apparently there are reproductive barriers that not only prevent the exchange of genes between well established species, but also between varieties of one and the same species. How these barriers arise is of central importance if one wants to understand the origin of biodiversity. A research team led by Detlef Weigel from the Max Planck Institute of Developmental Biology in Germany and Jeff Dangl from the University of North Carolina has now shown that a mis-regulated immune system can establish reproductive barriers and might be a first step toward speciation. The international collaboration studied a genetic incompatibility known as hybrid necrosis, using thale cress, Arabidopsis thaliana.
The new work, reported in PLoS Biology, was based on the observation that unfit hybrids from different plant species are very similar. Their growth is retarded, the leaves become yellow and necrotic, the tissue collapses and they often do not survive to make flowers; the syndrome is generally known as hybrid necrosis. "We suspected that hybrid necrosis is always caused by the same biochemical mechanism," explains Weigel, director at the Max Planck Institute.
To test this hypothesis, the scientists took 280 genetically different strains of Arabidopsis from all over the world, which they crossed in 861 different combinations. Most of the hybrid plants were strong and grew normally, but 20 - or two percent - of the crosses produced only small necrotic and unhealthy plants. Genomics-based experiments showed that these hybrids all had a comparable profile of gene activity:
A common group of some 1000 genes were either more strongly or more weakly active in the hybrids than in their healthy parents. Moreover, this pattern was very similar to what is seen with a strong immune response mounted against pathogens during a normal infection. The plant immune response typically involves the sacrifice of a few cells at and around the infection site. But in the wimpy hybrids, healthy tissue also suffered - without pathogen infection. The hybrid plants apparently mistook their own cells for dangerous germs.
Although the genes that determined the abnormal autoimmunity were different in most crosses, the researchers discovered that often only two genes were required to cause the necrotic hybrid response. One of the fatal genes came from the father, the other from the mother. In one case that the researchers studied in more detail, they found that the gene that causes necrosis in hybrids, but not in the parents, is normally used to sense the presence of a pathogen.
The scientists emphasize, however, that the hybrids are not the victims of malfunctioning genes: in contrast to many hereditary diseases, the necrosis is not due to each parent carrying a defective copy of the same gene. Rather, there is a destructive interaction between two different genes, each of which evolved differently in the two parents. The genes on their own are harmless or even beneficial, since the parents are healthy. Only the combination of the altered gene variants creates problems. These types of genetic malfunction are often known as Dobzhanshy-Muller incompatibilities, after the two giants of early modern genetics who first studied these necrotic hybrids in fruit flies.
The results of the German-American team challenge the classical definition of a species, according to which individuals of one species can mate at will and produce fertile offspring. Apparently there are barriers to the free interchange of genes even within a species; after all, one out of 50 crosses in this study was not successful. "The formation of new species thus needs to be understood as a gradual process, where barriers within a species continually increase, until two groups cannot be crossed at all anymore" says Weigel.
While this view is widely accepted today, it is mostly unclear, why such genetic barriers arise in the first place. Which advantage has the plant, when sometimes all seeds from a cross die? The current study offers a possible explanation. The plant genome changes under pressure from pathogens.
"Plant and pathogen are locked in a race," says Dangl, professor and expert in the genetics of plant pathology at the University of North Carolina. The pathogens tirelessly develop new strategies to attack the plant and evade its immune system. The plant, in turn, tries to be prepared against as many new microbe "weapons" as possible. Armed to the teeth, it can happen that a harmless protein variant from a more distant relative is all of a sudden classified as dangerous and attacked.
The scientists are optimistic that their insights can be applied to other species. Common traits indicate that hybrid necrosis in crops such as wheat is caused by the same mechanisms as in tale cress. Dangl therefore believes that Arabidopsis can serve as a useful model for the understanding of hybrid necrosis in general. "Such a model would be very useful for breeding, since such genetic incompatibilities prevents some of the crosses breeders would like to make," according to Dangl.
The finding that only a few genes are responsible for each case of hybrid necrosis is particularly encouraging. It seems that only a few genetic changes are required to circumvent crossing barriers und to achieve a desired new combination of genetic traits. The flip side of the coin is that only minimal modifications in the genome can be sufficient to suppress the free exchange of genes between relatives, and that perhaps not much is needed to form a new species.
Authors of the study were Detlef Weigel, Kirsten Bomblies, Janne Lempe, Norman Warthmann and Christa Lanz from the Max Planck Institute for Developmental Biology, Tübingen, Germany; and Petra Epple und Jeffery L. Dangl from the University of North Carolina in Chapel Hill, North Carolina, USA.
Reference: Detlef Weigel, Kirsten Bomblies, Janne Lempe, Norman Warthmann, Christa Lanz and Petra Epple und Jeffery L. Dangl "Autoimmune response as a mechanism for a Dobzhansky-Muller-type incompatibility syndrome in plants" PLoS Biology 5, e236 (4. September 2007)
Note: This story has been adapted from a news release issued by Max-Planck-Gesellschaft.

Fausto Intilla

www.oloscience.com

A Genetic Trigger For The Cambrian Explosion Unraveled?

Source:

http://www.sciencedaily.com/releases/2007/08/070831180409.htm

Science Daily — A team of scientists led by young Croatian evolutionary geneticist Tomislav Domazet-Lošo from Ruder Boškovic Institute (RBI) in Zagreb, Croatia, developed a novel methodological approach in evolutionary studies. Using the method they named 'genomic phylostratigraphy', its authors shed new and unexpected light on some of the long standing macroevolutionary issues, which have been puzzling evolutionary biologists since Darwin.

The only direct method of research in evolutionary history involves analyzing the fossil remains of once living organisms, excavated in various localities throughout of the world. However, that approach often cannot provide the full evolutionary pathway of some species, as it requires uncovering of many fossils from various stages of its evolutionary history. As the fossil record is imperfect, the evolution research fundamentally hinges on luck factor in discovering the adequate paleontological sites.
However, the RBI team proposed a novel and interesting approach to bypass this obstacle. Namely, they suggested that the genome of every extant species carries the ‘snapshots’ of evolutionary epochs that species went trough. What's even more important, they also developed the method which enables evolution researchers to readily convert those individual 'snapshots’ into the full-length 'evolutionary movie' of a species.
Applying their new methodology on the fruit fly genomic data they tackled some of the most intriguing evolutionary puzzles - some of which distressed even Darwin himself. First, they demonstrated that parts of the living organism exposed to the environment – so called ‘ectoderm’ - are more prone to evolutionary changes. Further, they explained the evolutionary origin of the ‘germ layers’, the primary tissue forms that form during the first days after the conception of a new animal, and from which subsequently all other tissues are developed. Finally, they discovered the potential genetic trigger for the 'Cambrian explosion', a major global evolutionary event on the planet, when some 540 million years ago almost all animal forms known today suddenly 'appeared'.
The first public lecture on these findings will be given by dr. Domazet-Lošo on September 4th at 5. ISABS Conference in Forensic Genetics and Molecular Anthropology, held in Split, Croatia. The groundbreaking paper fully presenting the theory of genomic phylostratigraphy will appear in the November issue of 'Trends in genetics', the most established monthly journal in Genetics.
Reference: Domazet-Lošo, T. et al. (2007) 'A phylostratigraphy approach to uncover the genomic history of major adaptations in metazoan lineages'. Trends in Genetics (to appear in the November 2007 issue of the journal)
Note: This story has been adapted from a news release issued by Rudjer Boskovic Institute.

Fausto Intilla

www.oloscience.com