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Summary
Viruses exert a major evolutionary force on their hosts, which has led to the emergence of host defensive and viral counter-defensive adaptations. Nowhere is this more evident than in the marine environment where 1023 viral infections to microbes are estimated to occur per second [1]. Viral lysis is an important contributor to the mortality of algae, which influences global nutrient cycles as phytoplankton contribute 50% of planetary primary production [2]. All known viruses that infect microscopic algae kill their host when they reproduce, releasing their viral offspring into the surrounding water. This is why it was surprising to find growing viruses in cultures of the marine green alga Ostreococcus [3]. As cultures started from a single cell, every cell should be identical to the others, so why were the susceptible cells not just killed-off by the virus and completely eliminated? By isolating susceptible and resistant single cells and tracking their growth both with and without viruses, my work has shown that some individuals occasionally changed between susceptible and resistant states. Few susceptible cells were enough to keep a growing viral population along-side a majority of viral-resistant algae. In Ostreococcus, host resistance to viruses was linked to rapid changes in the transcription pattern mainly restricted to one chromosome [4]. When cells switched between states, pieces would be lost from this chromosome, indicating it was these changes that helped cells to switch and that it functions as an “immunity chromosome”. A mathematic model describing the alga hedging its bets at each cell division—sometimes being susceptible and sometimes being resistant to viruses—matched what was seen in culture of algae and viruses multiplying together without any apparent drop in the overall population. Biologists often observe algal “bloom-and-bust” events, when algae form massive blooms that they can be visible from space but quickly die-off. This raises a big question: perhaps stable coexistence between algae and viruses is much more common, but it is simply not detected. I propose to study the genetic basis underlying algae–virus interactions by using Ostreococcus and its viruses as a model system with an approach integrating experimental evolution with joint host–virus genome-wide associations to determine the molecular bases of algae–virus coevolutionary dynamics both in the lab and in natural populations.
Brief biography
The common theme of my research is studying the function, ecology and evolution of microorganisms. I have worked at the level of single genes, single cells, populations and whole communities, using mainly "omics" technologies. My career began studying hydrocarbon-degrading Mycobacteria and the genetics of antibiotic resistance at the University of Sydney, Australia. I was interested in the (then) new movement of metagenomics, leading to my PhD at the University of New South Wales on the microbial ecology of Antarctic lakes. My most important discovery was that viruses act as the top predators in these lakes, as often multicellular life and unicellular grazers are rare or absent. This inspired me to continue studying host–virus interactions in environmental microorganisms, firstly as a post-doc in the Banyuls Oceanologic Observatory, France, then as a Juan de la Cierva Fellow at the Institute of Marine Sciences (ICM). I am now building on this theme as a CNRS (French National Centre for Scientific Research) researcher in the Evolutionary and Environmental Genomics of Phytoplankton (GENOPHY) group where I am focusing on interactions between marine green algae and viruses in the lab and the natural environment.
