ArticleGenetics2006
Regulation of DNA replication machinery by Mrc1 in fission yeast.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Transcriptional PBR cycles at pericentromeric repeats cause gross chromosomal rearrangements through Rad52-dependent ADR-loop formation.Nucleic acids research · 2026Article
- Hydroxyurea-The Good, the Bad and the Ugly.Genes · 2021Review
- The intra-S phase checkpoint directly regulates replication elongation to preserve the integrity of stalled replisomes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Time varying causal network reconstruction of a mouse cell cycle.BMC bioinformatics · 2019Article
- Genetic Interaction Landscape Reveals Critical Requirements for Schizosaccharomyces pombe Brc1 in DNA Damage Response Mutants.G3 (Bethesda, Md.) · 2015Article
- The CINs of the centromere.Biochemical Society transactions · 2013Review
- Phosphorylation of minichromosome maintenance protein 7 (MCM7) by cyclin/cyclin-dependent kinase affects its function in cell cycle regulation.The Journal of biological chemistry · 2013Article
- The fission yeast minichromosome maintenance (MCM)-binding protein (MCM-BP), Mcb1, regulates MCM function during prereplicative complex formation in DNA replication.The Journal of biological chemistry · 2013Article
- Abundance of prereplicative complexes (Pre-RCs) facilitates recombinational repair under replication stress in fission yeast.The Journal of biological chemistry · 2011Article
- Fission yeast Swi1-Swi3 complex facilitates DNA binding of Mrc1.The Journal of biological chemistry · 2010Article
- Hsk1 kinase and Cdc45 regulate replication stress-induced checkpoint responses in fission yeast.Cell cycle (Georgetown, Tex.) · 2010Article
- The role of specific checkpoint-induced S-phase transcripts in resistance to replicative stress.PloS one · 2009Article
- Perspectives on the DNA damage and replication checkpoint responses in Saccharomyces cerevisiae.DNA repair · 2009Review
- Replication fork reversal and the maintenance of genome stability.Nucleic acids research · 2009Review
- Mrc1 and DNA polymerase epsilon function together in linking DNA replication and the S phase checkpoint.Molecular cell · 2008Article
- Mcm4 C-terminal domain of MCM helicase prevents excessive formation of single-stranded DNA at stalled replication forks.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Expanded roles for Chk1 in genome maintenance.The Journal of biological chemistry · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Faithful replication of chromosomes is crucial to genome integrity. In yeast, the ORC binds replication origins throughout the cell cycle. However, Cdc45 binds these before S-phase, and, during replication, it moves along the DNA with MCM helicase. When replication progression is inhibited, checkpoint regulation is believed to stabilize the replication fork; the detailed mechanism, however, remains unclear. To examine the relationship between replication initiation and elongation defects and the response to replication elongation block, we used fission yeast mutants of Orc1 and Cdc45--orp1-4 and sna41-928, respectively--at their respective semipermissive temperatures with regard to BrdU incorporation. Both orp1 and sna41 cells exhibited HU hypersensitivity in the absence of Chk1, a DNA damage checkpoint kinase, and were defective in full activation of Cds1, a replication checkpoint kinase, indicating that normal replication is required for Cds1 activation. Mrc1 is required to activate Cds1 and prevent the replication machinery from uncoupling from DNA synthesis. We observed that, while either the orp1 or the sna41 mutation partially suppressed HU sensitivity of cds1 cells, sna41 specifically suppressed that of mrc1 cells. Interestingly, sna41 alleviated the defect in recovery from HU arrest without increasing Cds1 activity. In addition to sna41, specific mutations of MCM suppressed the HU sensitivity of mrc1 cells. Thus, during elongation, Mrc1 may negatively regulate Cdc45 and MCM helicase to render stalled forks capable of resuming replication.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.