{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Le AH"],"funding":["NIGMS NIH HHS"],"pagination":["728-38"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3711041"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2(7)"],"pubmed_abstract":["The DDK complex is a conserved kinase complex, consisting of a catalytic subunit, Hsk1 (Cdc7), and its regulatory subunit Dfp1 (Dbf4). This kinase is essential for DNA replication. In this work, we show that dfp1-r35, which truncates the Dfp1 C-terminus zinc finger, causes severe meiotic defects, including reduced spore viability, reduced formation of programmed double strand breaks, altered expression of meiotic genes, and disrupted chromosome segregation. There is a high frequency of dyad formation. Mutants are also defective in the phosphorylation and degradation of the meiotic cohesion, Rec8, resulting in a failure to proceed through the MII division. These defects are more pronounced in a haploid meiosis model than in a normal diploid meiosis. Thus, several critical meiotic functions are linked specifically to the C-terminus of Dfp1, which may target specific substrates for phosphorylation by Hsk1."],"journal":["Biology open"],"pubmed_title":["The C-terminus of S. pombe DDK subunit Dfp1 is required for meiosis-specific transcription and cohesin cleavage."],"pmcid":["PMC3711041"],"funding_grant_id":["R01 GM081418"],"pubmed_authors":["Le AH","Forsburg SL","Mastro TL"],"additional_accession":[]},"is_claimable":false,"name":"The C-terminus of S. pombe DDK subunit Dfp1 is required for meiosis-specific transcription and cohesin cleavage.","description":"The DDK complex is a conserved kinase complex, consisting of a catalytic subunit, Hsk1 (Cdc7), and its regulatory subunit Dfp1 (Dbf4). This kinase is essential for DNA replication. In this work, we show that dfp1-r35, which truncates the Dfp1 C-terminus zinc finger, causes severe meiotic defects, including reduced spore viability, reduced formation of programmed double strand breaks, altered expression of meiotic genes, and disrupted chromosome segregation. There is a high frequency of dyad formation. Mutants are also defective in the phosphorylation and degradation of the meiotic cohesion, Rec8, resulting in a failure to proceed through the MII division. These defects are more pronounced in a haploid meiosis model than in a normal diploid meiosis. Thus, several critical meiotic functions are linked specifically to the C-terminus of Dfp1, which may target specific substrates for phosphorylation by Hsk1.","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Jul","modification":"2024-11-20T23:01:09.533Z","creation":"2019-03-27T01:13:00Z"},"accession":"S-EPMC3711041","cross_references":{"pubmed":["23862021"],"doi":["10.1242/bio.20135173"]}}