Prolonged cell cycle arrest in response to DNA damage in yeast requires the maintenance of DNA damage signaling and the spindle assembly checkpoint.

ABSTRACT: Cells evoke the DNA damage checkpoint (DDC) to inhibit mitosis in the presence of DNA double-strand breaks (DSBs) to allow more time for DNA repair. In budding yeast, a single irreparable DSB is sufficient to activate the DDC and induce cell cycle arrest prior to anaphase for about 12-15 hr, after which cells 'adapt' to the damage by extinguishing the DDC and resuming the cell cycle. While activation of the DNA damage-dependent cell cycle arrest is well understood, how it is maintained remains unclear. To address this, we conditionally depleted key DDC proteins after the DDC was fully activated and monitored changes in the maintenance of cell cycle arrest. Degradation of Ddc2^ATRIP, Rad9, Rad24, or Rad53^CHK2 results in premature resumption of the cell cycle, indicating

SUBMITTER: Zhou FY 

PROVIDER: S-EPMC11630823 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature