Proliferating cells need to accurately duplicate and pass their genetic material on to daughter cells. Problems during replication and partition challenge the structural and numerical integrity of chromosomes. Diverse mechanisms, as the DNA replication checkpoint, survey the correct progression of replication and couple it with other cell cycle events to preserve genome integrity. The structural maintenance of chromosomes (SMC)
cohesin complex primarily contributes to
chromosome duplication by mediating the tethering of newly replicated sister chromatids, thus assisting their equal segregation in mitosis. In addition,
cohesin exerts important functions in genome organization, gene expression and DNA repair. These are determined by
cohesin's ability to bring together different
DNA segments and, hence, by the fashion and dynamics of its interaction with
chromatin. It recently emerged that
cohesin contributes to the protection of stalled replication forks through a mechanism requiring its timely mobilization from unreplicated
DNA and relocation to nascent strands. This mechanism relies on DNA replication checkpoint-dependent
cohesin ubiquitylation and promotes nascent sister chromatid entrapment, likely contributing to preserve stalled replisome-fork architectural integrity. Here we review how
cohesin dynamic association to
chromatin is controlled through post-translational modifications to dictate its functions during
chromosome duplication. We also discuss recent insights on the mechanism that mediates interfacing of replisome components with
chromatin-bound
cohesin and its contribution to the establishment of sister chromatid cohesion and the protection of stalled replication forks.