During cell proliferation, newly replicated sister chromatids must be pulled apart and correctly positioned in opposite cell halves before division for faithful transmission of genetic information. In eukaryotes, segregation only occurs after replication has been fully achieved. The pairing of sister chromatids during S and G2 phase is termed Sister Chromatid Cohesion (SCC). SCC is mediated by the cohesins, a multi-subunit complex composed of Structural Maintenance of Chromosomes (SMC) proteins, which are deposited behind replication forks2. In contrast, replication and segregation are concomitant in bacteria. Bacterial chromosomes harbor a single origin of bidirectional replication, oriC, which defines two replication arms. As replication progresses along the two chromosomal arms, newly replicated loci migrate towards opposite cell halves. Pioneer microscopy observations showed that there is a lag of a few minutes between the time of replication of a locus and the segregation of the two resulting copies in Escherichia coli; the lag was subsequently associated with prolonged interactions between sister loci. Strictly speaking, bacteria lack an ortholog of cohesins. However, by analogy with eukaryotes, we will refer to this phenomenon as bacterial Sister Chromatid Cohesion (bSCC). Studies performed in different labs including the group of Partner 1 further suggested that segregation lags were in part due to the time Topo-IV took to remove catenation links (precatenanes) behind replication forks. We have recently demonstrated that bSCC becomes dependent on the induction of the recN gene product by the SOS response when DNA is damaged. Remarkably, RecN is a SMC protein, suggesting that its action might be similar to eukaryotic cohesins. The discovery of a first positive bSCC factor that extends cohesion in the presence of DNA damages suggests that, as SCC in eukaryotes, bSCC is an important aspect of the cell cycle that can be remodeled according to the growth conditions and influence the next events of this cycle. These observations led Partner 3 to develop a new tool, Hi-SC2, to survey bSCC at the genome level in different growth conditions. The BaCh project stems from our first Hi-SC2 results in V. cholera revealing that many cohesion factors are yet to be found, which might act at specific genomic positions, in specific environmental circumstances and by different mechanisms. The consortium pursues 3 objectives related to the characterization of basal post replicative and DNA damage induced induced cohesions: (1) characterise of bSSC factors in bacterial genomes, (2) characterise their mechanism of action at the molecular level and (3) determine the roles that cohesion might play in the bacterial cell cycle in normal or perturbed conditions. To reach these objectives BaCh will rely on state of the art genomics, genetics, live cell imaging and single molecule biophysics assays.Tools developped during BaCh should be highly valuable for the sisster chromatid cohesion field in various organisms. In addition, we believe that the BaCh project should help unmask primary overarching cohesion mechanisms, which are still at work in all cellular life forms. In this regard, comparison of E. coli and V. cholerae, two bacteria that share many potential bSCC factors but display very different DNA replication and segregation cycles, will be particularly informative.