ArticleMolecular and cellular biology1997
Rfc5, a replication factor C component, is required for regulation of Rad53 protein kinase in the yeast checkpoint pathway.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 92 citations in OpenAlex.
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- Subunit Interaction Differences Between the Replication Factor C Complexes inFrontiers in plant science · 2018Article
- The unstructured C-terminal tail of yeast Dpb11 (human TopBP1) protein is dispensable for DNA replication and the S phase checkpoint but required for the G2/M checkpoint.The Journal of biological chemistry · 2011Article
- Genomic phenotyping of the essential and non-essential yeast genome detects novel pathways for alkylation resistance.BMC systems biology · 2011Article
- Perspectives on the DNA damage and replication checkpoint responses in Saccharomyces cerevisiae.DNA repair · 2009Review
- Mrc1 and DNA polymerase epsilon function together in linking DNA replication and the S phase checkpoint.Molecular cell · 2008Article
- Association of Rad9 with double-strand breaks through a Mec1-dependent mechanism.Molecular and cellular biology · 2004Article
- Biochemical characterization of DNA damage checkpoint complexes: clamp loader and clamp complexes with specificity for 5' recessed DNA.PLoS biology · 2003Article
- Rad53 phosphorylation site clusters are important for Rad53 regulation and signaling.Molecular and cellular biology · 2003Article
- Characterization of all the subunits of replication factor C from a higher plant, rice (Oryza sativa L.), and their relation to development.Plant molecular biology · 2003Article
- Elg1 forms an alternative RFC complex important for DNA replication and genome integrity.The EMBO journal · 2003Article
- Mrc1 is a replication fork component whose phosphorylation in response to DNA replication stress activates Rad53.Genes & development · 2003Article
- Mechanical link between cohesion establishment and DNA replication: Ctf7p/Eco1p, a cohesion establishment factor, associates with three different replication factor C complexes.Molecular and cellular biology · 2003Article
- Colocalization of human Rad17 and PCNA in late S phase of the cell cycle upon replication block.Oncogene · 2002Article
- Suppression of genome instability by redundant S-phase checkpoint pathways in Saccharomyces cerevisiae.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Topoisomerase III acts upstream of Rad53p in the S-phase DNA damage checkpoint.Molecular and cellular biology · 2001Article
- MCM2-7 proteins are essential components of prereplicative complexes that accumulate cooperatively in the nucleus during G1-phase and are required to establish, but not maintain, the S-phase checkpoint.Molecular biology of the cell · 2001Article
- Chl12 (Ctf18) forms a novel replication factor C-related complex and functions redundantly with Rad24 in the DNA replication checkpoint pathway.Molecular and cellular biology · 2001Article
- Loss of cell cycle checkpoint control in Drosophila Rfc4 mutants.Molecular and cellular biology · 2001Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RFC5 gene encodes a small subunit of replication factor C (RFC) complex in Saccharomyces cerevisiae. We have previously shown that a temperature-sensitive (ts) rfc5-1 mutation is impaired in the S-phase checkpoint. In this report, we show that the rfc5-1 mutation is sensitive to DNA-damaging agents. RFC5 is necessary for slowing the S-phase progression in response to DNA damage. The phosphorylation of the essential central transducer, Rad53 protein kinase, is reduced in response to DNA damage in rfc5-1 mutants during the S phase. Furthermore, the inducibility of RNR3 transcription in response to DNA damage is dependent on RFC5. It has been shown that phosphorylation of Rad53 is controlled by Mec1 and Tel1, members of the subfamily of ataxia-telangiectasia mutated (ATM) kinases. We also demonstrate that overexpression of TEL1 suppresses the ts growth defect and DNA damage sensitivity of rfc5-1 mutants and restores phosphorylation of Rad53 and RNR3 induction in response to DNA damage in rfc5-1. Our results, together with the observation that overexpression of RAD53 suppresses the defects of the rfc5-1 mutation, suggest that Rfc5 is part of a mechanism transducing the DNA damage signal to the activation of the central transducer Rad53.
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