<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>32(24)</volume><submitter>Manfrini N</submitter><pubmed_abstract>The Mec1 and Rad53 protein kinases are essential for budding yeast cell viability and are also required to activate the S-phase checkpoint, which supports DNA replication under stress conditions. Whether these two functions are related to each other remains to be determined, and the nature of the replication stress-dependent lethality of mec1 and rad53 mutants is still unclear. We show here that a decrease in cyclin-dependent kinase 1 (Cdk1) activity alleviates the lethal effects of mec1 and rad53 mutations both in the absence and in the presence of replication stress, indicating that the execution of a certain Cdk1-mediated event(s) is detrimental in the absence of Mec1 and Rad53. This lethality involves Cdk1 functions in both G(1) and mitosis. In fact, delaying either the G(1)/S transiti</pubmed_abstract><journal>Molecular and cellular biology</journal><pagination>4971-85</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3510536</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>G(1)/S and G(2)/M cyclin-dependent kinase activities commit cells to death in the absence of the S-phase checkpoint.</pubmed_title><pmcid>PMC3510536</pmcid><pubmed_authors>Trovesi C</pubmed_authors><pubmed_authors>Gobbini E</pubmed_authors><pubmed_authors>Lucchini G</pubmed_authors><pubmed_authors>Manfrini N</pubmed_authors><pubmed_authors>Longhese MP</pubmed_authors><pubmed_authors>Baldo V</pubmed_authors></additional><is_claimable>false</is_claimable><name>G(1)/S and G(2)/M cyclin-dependent kinase activities commit cells to death in the absence of the S-phase checkpoint.</name><description>The Mec1 and Rad53 protein kinases are essential for budding yeast cell viability and are also required to activate the S-phase checkpoint, which supports DNA replication under stress conditions. Whether these two functions are related to each other remains to be determined, and the nature of the replication stress-dependent lethality of mec1 and rad53 mutants is still unclear. We show here that a decrease in cyclin-dependent kinase 1 (Cdk1) activity alleviates the lethal effects of mec1 and rad53 mutations both in the absence and in the presence of replication stress, indicating that the execution of a certain Cdk1-mediated event(s) is detrimental in the absence of Mec1 and Rad53. This lethality involves Cdk1 functions in both G(1) and mitosis. In fact, delaying either the G(1)/S transiti</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Dec</publication><modification>2025-05-29T22:28:38.075Z</modification><creation>2025-05-29T22:28:38.075Z</creation></dates><accession>S-EPMC3510536</accession><cross_references><pubmed>23045388</pubmed><doi>10.1128/mcb.00956-12</doi><doi>10.1128/MCB.00956-12</doi></cross_references></HashMap>