ArticleMolecular biology of the cell2012
Colocalization of Mec1 and Mrc1 is sufficient for Rad53 phosphorylation in vivo.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Article
- The DNA damage checkpoint: A tale from budding yeast.Frontiers in genetics · 2022Review
- Review
- Separable functions of Tof1/Timeless in intra-S-checkpoint signalling, replisome stability and DNA topological stress.Nucleic acids research · 2020Article
- Hof1 plays a checkpoint-related role in MMS-induced DNA damage response inMolecular biology of the cell · 2020Article
- A role for the yeast PCNA unloader Elg1 in eliciting the DNA damage checkpoint.Current genetics · 2020Review
- Ddc2ATRIP promotes Mec1ATR activation at RPA-ssDNA tracts.PLoS genetics · 2019Article
- The Yeast PCNA Unloader Elg1 RFC-Like Complex Plays a Role in Eliciting the DNA Damage Checkpoint.mBio · 2019Article
- Mutations in Replicative Stress Response Pathways Are Associated with S Phase-specific Defects in Nucleotide Excision Repair.The Journal of biological chemistry · 2016Article
- Mcm2-7 Is an Active Player in the DNA Replication Checkpoint Signaling Cascade via Proposed Modulation of Its DNA Gate.Molecular and cellular biology · 2015Article
- Article
- Article
- Ddc2 mediates Mec1 activation through a Ddc1- or Dpb11-independent mechanism.PLoS genetics · 2014Article
- Article
- The DNA damage checkpoint response to replication stress: A Game of Forks.Frontiers in genetics · 2013Article
- Preserving Yeast Genetic Heritage through DNA Damage Checkpoint Regulation and Telomere Maintenance.Biomolecules · 2012Article
- The Multifaceted Role of Rad9 in the DNA Damage Response of Saccharomyces cerevisiae.Yeast (Chichester, England)Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
When DNA is damaged or DNA replication goes awry, cells activate checkpoints to allow time for damage to be repaired and replication to complete. In Saccharomyces cerevisiae, the DNA damage checkpoint, which responds to lesions such as double-strand breaks, is activated when the lesion promotes the association of the sensor kinase Mec1 and its targeting subunit Ddc2 with its activators Ddc1 (a member of the 9-1-1 complex) and Dpb11. It has been more difficult to determine what role these Mec1 activators play in the replication checkpoint, which recognizes stalled replication forks, since Dpb11 has a separate role in DNA replication itself. Therefore we constructed an in vivo replication-checkpoint mimic that recapitulates Mec1-dependent phosphorylation of the effector kinase Rad53, a crucial step in checkpoint activation. In the endogenous replication checkpoint, Mec1 phosphorylation of Rad53 requires Mrc1, a replisome component. The replication-checkpoint mimic requires colocalization of Mrc1-LacI and Ddc2-LacI and is independent of both Ddc1 and Dpb11. We show that these activators are also dispensable for Mec1 activity and cell survival in the endogenous replication checkpoint but that Ddc1 is absolutely required in the absence of Mrc1. We propose that colocalization of Mrc1 and Mec1 is the minimal signal required to activate the replication checkpoint.
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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.