ArticleCell cycle (Georgetown, Tex.)2014
Mcm10 deficiency causes defective-replisome-induced mutagenesis and a dependency on error-free postreplicative repair.
Article in Cell cycle (Georgetown, Tex.), 2014. 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.
- Stabilization of expandable DNA repeats by the replication factor Mcm10 promotes cell viability.Nature communications · 2024Article
- MCM10 expression is linked to cervical cancer aggressiveness.Frontiers in molecular medicine · 2023Article
- Post-Translational Modifications of PCNA: Guiding for the Best DNA Damage Tolerance Choice.Journal of fungi (Basel, Switzerland) · 2022Review
- Review
- Recombination and Pol ζ Rescue Defective DNA Replication upon Impaired CMG Helicase-Pol ε Interaction.International journal of molecular sciences · 2020Article
- DNA Polymerases at the Eukaryotic Replication Fork Thirty Years after: Connection to Cancer.Cancers · 2020Review
- Review
- Flap endonuclease overexpression drives genome instability and DNA damage hypersensitivity in a PCNA-dependent manner.Nucleic acids research · 2018Article
- The importance of an interaction network for proper DNA polymerase ζ heterotetramer activity.Current genetics · 2018Review
- Review
- Yeast DNA polymerase ζ maintains consistent activity and mutagenicity across a wide range of physiological dNTP concentrations.Nucleic acids research · 2017Article
- Gata6 promotes hair follicle progenitor cell renewal by genome maintenance during proliferation.The EMBO journal · 2017Article
- Mapping ubiquitination sites ofBiochemistry and biophysics reports · 2016Article
- Xenopus Mcm10 is a CDK-substrate required for replication fork stability.Cell cycle (Georgetown, Tex.) · 2016Article
- Slx5/Slx8 Promotes Replication Stress Tolerance by Facilitating Mitotic Progression.Cell reports · 2016Article
- Genetic Interactions Implicating Postreplicative Repair in Okazaki Fragment Processing.PLoS genetics · 2015Article
- Mcm10 is required for oogenesis and early embryogenesis in Drosophila.Mechanisms of development · 2015Article
- Error-free DNA damage tolerance and sister chromatid proximity during DNA replication rely on the Polα/Primase/Ctf4 Complex.Molecular cell · 2015Article
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Authors and funding
4 authors.
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Abstract
Mcm10 is a multifunctional replication factor with reported roles in origin activation, polymerase loading, and replication fork progression. The literature supporting these variable roles is controversial, and it has been debated whether Mcm10 has an active role in elongation. Here, we provide evidence that the mcm10-1 allele confers alterations in DNA synthesis that lead to defective-replisome-induced mutagenesis (DRIM). Specifically, we observed that mcm10-1 cells exhibited elevated levels of PCNA ubiquitination and activation of the translesion polymerase, pol-ζ. Whereas translesion synthesis had no measurable impact on viability, mcm10-1 mutants also engaged in error-free postreplicative repair (PRR), and this pathway promoted survival at semi-permissive conditions. Replication gaps in mcm10-1 were likely caused by elongation defects, as dbf4-1 mutants, which are compromised for origin activation did not display any hallmarks of replication stress. Furthermore, we demonstrate that deficiencies in priming, induced by a pol1-1 mutation, also resulted in DRIM, but not in error-free PRR. Similar to mcm10-1 mutants, DRIM did not rescue the replication defect in pol1-1 cells. Thus, it appears that DRIM is not proficient to fill replication gaps in pol1-1 and mcm10-1 mutants. Moreover, the ability to correctly prime nascent DNA may be a crucial prerequisite to initiate error-free PRR.
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