We use Chlamydomonas to try to understand how a unicellular organism adapts to survive in a hostile environment. If it has already been shown that in the face of a strong stress Chlamydomonas can trigger programmed cell death (PCD), we have discovered in our team that in response to more moderate stresses, cells aggregate forming impressive multicellular structures in which algae can be protected from the toxic environment. We are trying to uncover the mechanisms that control both PCD and aggregation in Chlamydomonas.

Chlamydomonas reinhardtii is the most prominent model organism in the green algae lineage for both basic research and biotechnological applications. We use Chlamydomonas to try to understand how a unicellular organism adapts to survive in a hostile environment. Although some experiments indicate the existence of programmed cell death (PCD) in response to severe stresses in Chlamydomonas, the mechanisms controlling this process and the signaling pathways involved, have yet to be identified (de Carpentier et al., 2019).

Excitingly, we have shown recently that Chlamydomonas cells that self-destruct emit molecules in the culture medium that allow better resistance and survival of other cells in the population, highlighting the existence of altruistic mechanisms. We have also discovered that in response to more moderate stresses, cells aggregate forming multicellular structures in which algae can be protected.

Cellular aggregation would be an intermediate stage where the stress is not strong enough to induce PCD, but where nevertheless cells collaborate to protect themselves. As Chlamydomonas is amenable to powerful genetic approaches, we have built an insertional mutant library, from which we have identified two families of original mutants: the survivor (sur) mutants which are no longer triggering PCD in response to several stresses, and the socializer (saz) mutants that form aggregates spontaneously. We have identified the genes affected in most of these mutants. Further characterization of the mutants by RNA-Seq and quantitative proteomic studies has been performed and allowed us to have a better overview of the mechanisms controlling PCD and aggregation in Chlamydomonas. Our multi-omics approach led us to identify potential key regulators of PCD and aggregation in Chlamydomonas. These candidates are then tested for their involvement in the aggregation or PCD using mutants obtained from the Chlamydomonas Library Project (CLiP) (Li et al., 2019).

Since the dynamics and mode of formation of multicellular structures in Chlamydomonas are very poorly known, we are also developing microfluidic tools that allow us to follow this process in detail over a period of time ranging from several hours to several days. Some of the candidates we have identified in our multi-omics studies can be fused to specific fluorescent proteins, using tools developed in our lab (Crozet et al., 2018; de Carpentier et al., 2020), to follow their movement during the same period, and to highlight their potential role. The aggregation of cells over a long period of time is one of the hypotheses classically formulated to explain the transition from unicellularity to multicellularity over the course of evolution.

Our research on the mechanisms leading to aggregation in response to stress and the characterization of saz mutants could therefore also contribute to a better understanding of the appearance of multicellularity in Volvocales.

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