Virginia LIOY: Functional reorganization of Salmonella chromatin during virulence expression: new insights into H-NS counter silencing (Séminaire invité CRP)

Virginia LIOY

Chercheuse à l'I2BC Paris Saclay, Département "Biologie des génomes", Equipe "Conformation et ségrégation du chromosome bactérien" dirigée par Frédéric Boccard

The genomes of all living organisms are large molecules that have to be highly compacted to fit inside cells whose size is a thousand times smaller. This compaction has, at the same time, to be accessible to all the essential biological processes that allow bacteria to replicate, maintain, and express their genomes. Recent studies have shown that bacterial chromosomes are organized in a dynamic and multiscale manner by Nucleoid-Associated Proteins (NAPs) and condensin complexes. Within this structuration, NAPs are master operators working at different scales of organization. Additionally, some NAPs can regulate gene expression. In Salmonella, the NAP H-NS silences the Salmonella Pathogenicity Islands (SPIs), which are horizontally acquired genetic elements that allow this bacterium to infect and survive within host cells. SPIs are counter-silenced at a precise moment of the Salmonella infectious cycle. The changes in SPI chromatin structure and the precise contribution of regulatory factors to these changes are poorly characterized. We studied silenced SPI chromatin and the structural changes followed by SPI-1 chromatin upon H-NS counter-silencing. Our results show that within silent SPIs, H-NS binding is correlated with a significant level of transcriptional activity and RNA polymerase occupancy, but without preferential interactions between SPI genes. When SPI-1 is expressed, chromatin shows a variable distribution of H-NS occupancy, with H-NS-free regions, but also with invariable regions. Interestingly, we observe a drastic re-organization of SPI-1 chromatin into transcriptionally induced domains (TIDs) in a HilD-dependent manner. Overall, we propose a model in which the switches from silent to active SPI-1 chromatin evolved to enable the functional regulation of this pathogenicity island