ArticleBioEssays : news and reviews in molecular, cellular and developmental biology2014
Genetic instability is prevented by Mrc1-dependent spatio-temporal separation of replicative and repair activities of homologous recombination: homologous recombination tolerates replicative stress by Mrc1-regulated replication and repair activities operating at S and G2 in distinct subnuclear compartments.
Article in BioEssays : news and reviews in molecular, cellular and developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Effect and mechanism of signal peptide and maltose on recombinant type III collagen production in Pichia pastoris.Applied microbiology and biotechnology · 2023Article
- Timing of Chromosome DNA Integration throughout the Yeast Cell Cycle.Biomolecules · 2023Article
- Mrc1-Dependent Chromatin Compaction Represses DNA Double-Stranded Break Repair by Homologous Recombination Upon Replication Stress.Frontiers in cell and developmental biology · 2021Article
- Homologous Recombination: To Fork and Beyond.Genes · 2018Review
- Multi-Invasion-Induced Rearrangements as a Pathway for Physiological and Pathological Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018Review
- Mutations in the Non-Catalytic Subunit Dpb2 of DNA Polymerase Epsilon Affect the Nrm1 Branch of the DNA Replication Checkpoint.PLoS genetics · 2017Article
- Homologous recombination maintenance of genome integrity during DNA damage tolerance.Molecular & cellular oncologyReview
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Abstract
Homologous recombination (HR) is required to protect and restart stressed replication forks. Paradoxically, the Mrc1 branch of the S phase checkpoints, which is activated by replicative stress, prevents HR repair at breaks and arrested forks. Indeed, the mechanisms underlying HR can threaten genome integrity if not properly regulated. Thus, understanding how cells avoid genetic instability associated with replicative stress, a hallmark of cancer, is still a challenge. Here I discuss recent results that support a model by which HR responds to replication stress through replicative and repair activities that operate at different stages of the cell cycle (S and G2, respectively) and in distinct subnuclear structures. Remarkably, the replication checkpoint appears to control this scenario by inhibiting the assembly of HR repair centers at stressed forks during S phase, thereby avoiding genetic instability.
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