Just a quick announcement for a 1-week summer school of bioinformatics in Bratislava, in which I will be lecturing. You can have more info here.
Here is a short description from the course website:
The summer school will provide an overview of several areas of computational biology, covering concrete tools, examples of their use, and underlying models and methods. Intended audience includes biologists who want to become more experienced bioinformatics users as well as computer scientists, mathematicians and others who are interested in this exciting research area. The summer school is primarily targeted at doctoral students and postdocs, although more experienced researchers or Master students are welcome to attend as well. The program will include lectures, practical workshops, and research seminars given by experienced researchers from several countries. Working language is English.
Sunday, May 1, 2011
Friday, March 18, 2011
The father of orthology and paralogy concepts, passes off.
Friday, February 11, 2011
On the debate of recognising mitochondria as bacteria
I recently read Mark Pallen's provocative opinion article on whether we should recognise mitochondria as bacteria, and therefore give them their own taxonomic classification (now they are simply considered an organelle of the host cell). This paper has been featured and discussed in other blogs such as that of Jonathan Eisen.
This issue is close to my heart, since I did my PhD precisely in tracing the origin and evolution of this organelles and their inter-mingling with their hosts. I agree with many of the arguments raised by Pallen,
but I do not necessarily conclude that this should lead us to create a distinct taxonomic class for mitochondria. In practice, thinking of "mitochondria as bacteria" can coexist with its current classification as an organelle, as long as we are aware of their bacterial ancestry. Indeed I think that this is the dominant view of most people doing research on mitochondria, so I do not think that classifying mitochondria as a new bacterial class will radically enhance our possibilities of understanding or manipulating this organelles. On the other hand one could argue that strictly considering mitochondria as bacteria will close our eyes to the critical organellar properties of mitochondria, thereby hampering our potential to understand them. I imagine a future opinion paper entitled "time to recognise that Mitochondriaceae are organelles?", with the same kind of arguments arguing for recognising mitochondria as a true organelle from the host cells, and listing its many similarities with other membrane-bounded organelles in the cell.
Since evolution has crossed the border from free living bacterium to organelle at least a couple of times, it follows that these two stages are united by a continued evolutionary time line, of small stages separated by a discrete number of changes. The current diversity only allows us to infer some of these intermediate stages and usually these are used to base our "categories". Making a separation is of course arbitrary but useful to describe to things that appear different to us. Despite the parallelisms mentioned with some reduced endosymbiont or pathogens, there is a quantitative jump in the level of integration with the host cell that we can easily recognize. Setting there a divide between what we call an organelle or what we call a bacterial species seems to me reasonable, although we could think of other operational definitions, is clear.
All the rest is deciding what degree of purity we want to apply to our definitions. As a biologist I am used to the limitations of our central concepts such as the ones of "species" or "genes", which similarly have to accomodate exceptions and different interpretations depending on what organisms we are dealing with. We humans have a natural tendency of classifying things into simple schemes, and we have to recognize the advantage of using operational classifications that are "generally correct" while not becoming too uneasy when understanding that the actual complexity is much bigger. The important thing is to be aware of the exceptions and of the "provisional and approximate nature" of practical definitions, until we find better ones.
In summary, I am in favour of changes of our current paradigms to newer ones that better fit our current knowledge, but I am of the opinion that simply giving mitochondria the level of a taxonomic family is not solving anything, nor improving our understanding of these "highly derived bacteria" or "bacterial-derived organelles", as you prefer to call them.
but I do not necessarily conclude that this should lead us to create a distinct taxonomic class for mitochondria. In practice, thinking of "mitochondria as bacteria" can coexist with its current classification as an organelle, as long as we are aware of their bacterial ancestry. Indeed I think that this is the dominant view of most people doing research on mitochondria, so I do not think that classifying mitochondria as a new bacterial class will radically enhance our possibilities of understanding or manipulating this organelles. On the other hand one could argue that strictly considering mitochondria as bacteria will close our eyes to the critical organellar properties of mitochondria, thereby hampering our potential to understand them. I imagine a future opinion paper entitled "time to recognise that Mitochondriaceae are organelles?", with the same kind of arguments arguing for recognising mitochondria as a true organelle from the host cells, and listing its many similarities with other membrane-bounded organelles in the cell.
Since evolution has crossed the border from free living bacterium to organelle at least a couple of times, it follows that these two stages are united by a continued evolutionary time line, of small stages separated by a discrete number of changes. The current diversity only allows us to infer some of these intermediate stages and usually these are used to base our "categories". Making a separation is of course arbitrary but useful to describe to things that appear different to us. Despite the parallelisms mentioned with some reduced endosymbiont or pathogens, there is a quantitative jump in the level of integration with the host cell that we can easily recognize. Setting there a divide between what we call an organelle or what we call a bacterial species seems to me reasonable, although we could think of other operational definitions, is clear.
All the rest is deciding what degree of purity we want to apply to our definitions. As a biologist I am used to the limitations of our central concepts such as the ones of "species" or "genes", which similarly have to accomodate exceptions and different interpretations depending on what organisms we are dealing with. We humans have a natural tendency of classifying things into simple schemes, and we have to recognize the advantage of using operational classifications that are "generally correct" while not becoming too uneasy when understanding that the actual complexity is much bigger. The important thing is to be aware of the exceptions and of the "provisional and approximate nature" of practical definitions, until we find better ones.
In summary, I am in favour of changes of our current paradigms to newer ones that better fit our current knowledge, but I am of the opinion that simply giving mitochondria the level of a taxonomic family is not solving anything, nor improving our understanding of these "highly derived bacteria" or "bacterial-derived organelles", as you prefer to call them.
Wednesday, February 9, 2011
EMBO-meeting Comparative Genomics of Eukaryotic Microorganisms
This is a quick note to announce this year's EMBO meeting on: Comparative genomics of eukaryotic microorganisms: understanding the complexity of diversity
I have attended to this meeting since 2006 and always enjoyed it. Besides the impressive panel of speakers there is plenty of time to meet with all attendees in an informal environment, so is one of this fruitful meeting from which you return with a broader knowledge and new ideas. Recommended.
15 - 20 October | 2011 | Sant Feliux | Spain
Sunday, January 30, 2011
Why only hungry K.lactis have sex?
One of my professors at the Univeristy of Valencia used to tell us that a Yeast's life was "mainly driven by food and sex", referring to the relevance and impact in this single-cell organisms of the signalling pathways in response to starvation, presence of nutrients or pheromones. One particular species of yeast, the diary yeast Kluyveromyces lactis, seemed to have combined both stimuli into a single pathway, requiring both starvation and pheromone signals to mate. Although this was known for decades, the specific mechanism and how it had evolved remained a mystery.
In a recent paper by the group of Alexander Johnson (UCSF), the origin of such phenotype has been established, by comparing regulation of mating genes in K. lactis, Saccharomyces cerevisiae, and Candida albicans. The evolutionary mechanism involved is that of a transcriptional rewiring, in which the core mating genes have been put under the control of the gene responsible for signalling starvation (RME1), which in turn is now also controlled by the mating factors (a/alpha). This intercalation of a new step within the mating signalling pathway effectively results in both stimuli being necessary for mating.
How could this happen? the implied scenario involves the acquisition of regulation by mating factors for RME1, at least four core mating genes loosing their reponsive elements to the mating factors - rather than change of the binding site of the factor, which was found to be similar to that in the other yeasts-, and the same genes acquiring responsive elements to RME1. 9 transitions in total. The first one (RME1 under control of mating) also occurs in S. cerevisiae, so it seems to have pre-dated the re-programming of the core mating genes control, effectively paving the way for the final rewiring. To unveil the order of the other 8 transitions, one would need to find intermediate states in other yeasts. Given the potential deleterious effects of a mating gene loosing pheromone control, and the low probability of loosing one binding factor while acquiring the other one in four genes, I envision an intermediary state where the genes where responding to both RME1/mating factors. Then, the lost in a single core mating gene of the direct response to mating factors would render the pheromone-responsive elements in the other core genes non-functional (three of this core genes encode proteins that should be combined into a heterotrimer to function), thus leaving the only functional route that passing through RME1. Accumulating mutations would have then simply removed the pheromone-response site.
An interesting story of how regulation can effectively be altered by evolution in small steps. Another important connection is that of the fact that for many fungi, most particularly pathogens such as Candida glabrata, we lack direct observation of the mating cycle although they conserve intact the mating genes and for some we have indirect evidence that they mate. Perhaps it all comes down to very specific requirements for mating, achieved by intercalating layers of regulation of mating genes as that found in K. lactis.
How could this happen? the implied scenario involves the acquisition of regulation by mating factors for RME1, at least four core mating genes loosing their reponsive elements to the mating factors - rather than change of the binding site of the factor, which was found to be similar to that in the other yeasts-, and the same genes acquiring responsive elements to RME1. 9 transitions in total. The first one (RME1 under control of mating) also occurs in S. cerevisiae, so it seems to have pre-dated the re-programming of the core mating genes control, effectively paving the way for the final rewiring. To unveil the order of the other 8 transitions, one would need to find intermediate states in other yeasts. Given the potential deleterious effects of a mating gene loosing pheromone control, and the low probability of loosing one binding factor while acquiring the other one in four genes, I envision an intermediary state where the genes where responding to both RME1/mating factors. Then, the lost in a single core mating gene of the direct response to mating factors would render the pheromone-responsive elements in the other core genes non-functional (three of this core genes encode proteins that should be combined into a heterotrimer to function), thus leaving the only functional route that passing through RME1. Accumulating mutations would have then simply removed the pheromone-response site.
An interesting story of how regulation can effectively be altered by evolution in small steps. Another important connection is that of the fact that for many fungi, most particularly pathogens such as Candida glabrata, we lack direct observation of the mating cycle although they conserve intact the mating genes and for some we have indirect evidence that they mate. Perhaps it all comes down to very specific requirements for mating, achieved by intercalating layers of regulation of mating genes as that found in K. lactis.
Friday, January 28, 2011
Map of scientific collaborations
My brother pointed to me this map of scientific collaboration between researchers made by Olivier H. Beauchesne. Inspired by a similar map drawn for facebook friends, O. Beauchesne used a bibliographical database to trace links between universities if their respective researchers were co-authoring articles.
The result is an amazing picture, that shows that, as for many other things, research is unevenly distributed around the world. With a clear North/South divide, research and economic centres overlap almost completely. As expected, North-america, Europe and Japan are the most densely connected areas. Emerging research countries such as India, China, and Brasil can also be recognized. Within Europe, South UK, Paris, the Netherlands, and Switzerland/Austria seem to form research hubs. Perhaps influenced by language and cultural ties, Spain and Portugal are relatively well connected to central and south-American countries.
Barcelona, where my lab is located, appears to be the most densely connected research pole in Spain.
Barcelona, where my lab is located, appears to be the most densely connected research pole in Spain.
Wednesday, January 19, 2011
A PLoS currents for the Tree of Life
I recently discovered that PLoS Currents has opened a new track for the Tree of Life: PLoS Currents: Tree Of Life.
PLoS currents is yet another form of publishing scientific results. A small group of editors and reviewers reviews every paper to check that it is t is " a legitimate work of science and does not contain any obvious methodological, ethical or legal violations." If that's the case papers are published immediately (and indexed in Pubmed). Another novelty is that all the publication procedure is based on a web-based tool called google-knol.
So far there are only 4 articles (or "knols"?) and they all seem pertinent to the topic, one of them was very useful to me, since it described a compilation of benchmark datasets for phylogeny.
It looks worth to keep an eye.
PLoS currents is yet another form of publishing scientific results. A small group of editors and reviewers reviews every paper to check that it is t is " a legitimate work of science and does not contain any obvious methodological, ethical or legal violations." If that's the case papers are published immediately (and indexed in Pubmed). Another novelty is that all the publication procedure is based on a web-based tool called google-knol.
So far there are only 4 articles (or "knols"?) and they all seem pertinent to the topic, one of them was very useful to me, since it described a compilation of benchmark datasets for phylogeny.
It looks worth to keep an eye.
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