Preparation for DNA replication: the key to a successful S phase
نویسندگان
چکیده
منابع مشابه
DNA polymerase ϵ links the DNA replication machinery to the S phase checkpoint
Inhibition of DNA synthesis induces transcription of DNA damage-inducible genes and prevents mitotic entry through the action of the S phase checkpoint. We have isolated a mutant, dun2, defective for both of these responses. DUN2 is identical to POL2, encoding DNA polymerase ~ (pol ~). Unlike sad1 mutants defective for multiple cell cycle checkpoints, po12 mutants are defective only for the S p...
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Activation of a host DNA damage response (DDR) is essential for DNA replication of minute virus of canines (MVC), a member of the genus Bocavirus of the Parvoviridae family; however, the mechanism by which DDR contributes to viral DNA replication is unknown. In the current study, we demonstrate that MVC infection triggers the intra-S-phase arrest to slow down host cellular DNA replication and t...
متن کاملMcl1p Is a Polymerase Replication Accessory Factor Important for S-Phase DNA Damage Survival
Mcl1p is an essential fission yeast chromatin-binding protein that belongs to a family of highly conserved eukaryotic proteins important for sister chromatid cohesion. The essential function is believed to result from its role as a Pol1p (polymerase ) accessory protein, a conclusion based primarily on analogy to Ctf4p’s interaction with Pol1p. In this study, we show that Mcl1p also binds to Pol...
متن کاملDNA replication and spindle checkpoints cooperate during S phase to delay mitosis and preserve genome integrity
Deoxyribonucleic acid (DNA) replication and chromosome segregation must occur in ordered sequence to maintain genome integrity during cell proliferation. Checkpoint mechanisms delay mitosis when DNA is damaged or upon replication stress, but little is known on the coupling of S and M phases in unperturbed conditions. To address this issue, we postponed replication onset in budding yeast so that...
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ژورنال
عنوان ژورنال: FEBS Letters
سال: 2019
ISSN: 0014-5793,1873-3468
DOI: 10.1002/1873-3468.13619