High-throughput screening identifies a previously undescribed checkpoint controlling mitotic progression in response to DNA damage.

ABSTRACT: Following DNA damage, the cell cycle can be slowed or halted to allow for DNA repair. However, the mechanisms underpinning mitotic delay in response to DNA damage are unclear. Through an unbiased high-throughput screen, here, we have identified superoxide dismutase 1 (SOD1) as an essential factor mediating mitotic delay in response to DNA damage. Cells with damaged DNA arrest at metaphase, indicating involvement of the spindle assembly checkpoint (SAC); however, this response is lost following SOD1 depletion. Furthermore, whilst depletion of SAC proteins promotes rapid cell division (often less than 10 min) in all conditions, SOD1 depletion has no impact on mitotic progression either in unperturbed mitosis or in response to spindle poisons and does not decrease the mitotic transit time bey

SUBMITTER: Li N 

PROVIDER: S-EPMC12713330 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature