Ongoing replication forks delay the nuclear envelope breakdown upon mitotic entry.

ABSTRACT: DNA replication is a major contributor to genomic instability, and protection against DNA replication perturbation is essential for normal cell division. Certain types of replication stress agents, such as aphidicolin and hydroxyurea, have been shown to cause reversible replication fork stalling, wherein replisome complexes are stably maintained with competence to restart in the S phase of the cell cycle. If these stalled forks persist into the M phase without a replication restart, replisomes are disassembled in a p97-dependent pathway and under-replicated DNA is subjected to mitotic DNA repair synthesis. Here, using Xenopus egg extracts, we investigated the consequences that arise when stalled forks are released simultaneously with the induction of mitosis. Ara-cytidine-5'-triphosphate-i

SUBMITTER: Hashimoto Y 

PROVIDER: S-EPMC7948514 | biostudies-literature | 2021 Jan-Jun

REPOSITORIES: biostudies-literature