|Sébastien Verne's website|
I am mostly interested in the evolution of biological interactions, i.e. the interactions that occur between two or several living species. My researches are axed both on the underlying mecanisms that shape the biological interactions and on the evolutionary consequences of these interactions. Indeed, competition, mutualism, parasitism or predation constitute strong engines of the Evolution because they involve very diverse adaptations in the concerned organisms. For example, the relationships between a parasite and its host can drive to an evolutionary arms race: the natural selection will favor the parasites that are the fittest to find and to exploit their host. On the other side, the natural selection will favor the hosts that are the fittest to avoid the parasites and/or to resist to the parasites attacks. Sometimes, the evolution can lead to the emergence of mutualism between a parasite and its host because an early death of the host will lead to the death of the parasite too. As a consequence, the parasite should not be too virulent and the natural selection can favor the parasites that give a benefit to their host (e.g. a better resistance to other parasites or disease). Such evolution is impossible in predators because they usually have to kill their prey to eat it.
I am also very interested in the consequences of the biological interactions (particularly in the case of symbiosis) on the dynamic and population genetics. Indeed, because of their inheritence, some parasites, like the bacteria of the genus Wolbachia, will deeply affect the genetic structure of invertebrates populations that host them. Conversely, the connetivity (i.e. the migrations) of the host populations can influence the population dynamic of the parasites.
During my PhD work, I focused on an original and fascinating model constituted by a host and its reproductive parasite. Indeed, the terrestrial Isopod Armadillidium vulgare is one of the many species that host the bacteria Wolbachia. This bacteria is usually only transmitted via the eggs, from mother to the progeny. An infected male can not transmit the bacteria. To improve its fitness, Wolbachia will simply oblige the males to developp into females during the first weeks of the embryonnic development. My PhD work consisted in the analysis of the population genetic structure of A. vulgare to try to understand how it is affected by Wolbachia. It was also to understand how a given isopod population structure (e.g. isolated population or a metapopulation dynamic) could favor or limit the spread of Wolbachia within and between populations. This work is mainly based on population genetics approaches with the use of several kinds of genetic markers. However, it also needed behavioral experiments, and many rearings to compare the life history traits of several types of females (i.e. asymbiotic vs. infected females) and the host phenotype change induced by the bacteria.
During my postdoc in Vancouver (BC, western coast of Canada), I worked on a completely different model, as it was the couple of spruce (Picea spp.) and the white pine weevil (Pissodes strobi). The white pine weevil severly damages the North American conifer forests in attacking the leader shoots of the young trees. They often even kill the leader shoot of the tree. The consequences are a reduced growth, stem deformation (crook, fork) and a financial loss for the forest industry. During this work, I studied the genetic basis of spruce constitutive resistance to the weevil. To identify these basis, I used transcriptomic approaches (cDNA microarrays) and quantitative genetics (QTLs).
I am now looking for a new postdoc position in genomics to continue to work on long-term biological interactions (host-parasite or mutualistic), preferably in Western Europe.