ArticleThe Journal of biological chemistry2010
Loss of H3 K79 trimethylation leads to suppression of Rtt107-dependent DNA damage sensitivity through the translesion synthesis pathway.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- DOT1L Mediates Stem Cell Maintenance and Represents a Therapeutic Vulnerability in Cancer.Cancer research · 2025Review
- DOT1L and H3K79 Methylation in Transcription and Genomic Stability.Biomolecules · 2018Review
- Writing, erasing and reading histone lysine methylations.Experimental & molecular medicine · 2017Review
- Overexpression screens identify conserved dosage chromosome instability genes in yeast and human cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Review
- Dot1 histone methyltransferases share a distributive mechanism but have highly diverged catalytic properties.Scientific reports · 2015Article
- Interplay between histone H3 lysine 56 deacetylation and chromatin modifiers in response to DNA damage.Genetics · 2015Article
- Conditional genetic interactions of RTT107, SLX4, and HRQ1 reveal dynamic networks upon DNA damage in S. cerevisiae.G3 (Bethesda, Md.) · 2014Article
- Article
- The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle.Cell cycle (Georgetown, Tex.) · 2014Review
- Chromatin and the genome integrity network.Nature reviews. Genetics · 2013Review
- The yeast forkhead transcription factors fkh1 and fkh2 regulate lifespan and stress response together with the anaphase-promoting complex.PLoS genetics · 2012Article
- Diverse roles of RNA polymerase II-associated factor 1 complex in different subpathways of nucleotide excision repair.The Journal of biological chemistry · 2011Article
- Rtt107 is required for recruitment of the SMC5/6 complex to DNA double strand breaks.The Journal of biological chemistry · 2011Article
- The diverse functions of Dot1 and H3K79 methylation.Genes & development · 2011Review
- Evidence that the histone methyltransferase Dot1 mediates global genomic repair by methylating histone H3 on lysine 79.The Journal of biological chemistry · 2011Article
- The many faces of histone H3K79 methylation.Mutation research. Reviews in mutation researchReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Genomic integrity is maintained by the coordinated interaction of many DNA damage response pathways, including checkpoints, DNA repair processes, and cell cycle restart. In Saccharomyces cerevisiae, the BRCA1 C-terminal domain-containing protein Rtt107/Esc4 is required for restart of DNA replication after successful repair of DNA damage and for cellular resistance to DNA-damaging agents. Rtt107 and its interaction partner Slx4 are phosphorylated during the initial phase of DNA damage response by the checkpoint kinases Mec1 and Tel1. Because the natural chromatin template plays an important role during the DNA damage response, we tested whether chromatin modifications affected the requirement for Rtt107 and Slx4 during DNA damage repair. Here, we report that the sensitivity to DNA-damaging agents of rtt107Δ and slx4Δ mutants was rescued by inactivation of the chromatin regulatory pathway leading to H3 K79 trimethylation. Further analysis revealed that lack of Dot1, the H3 K79 methyltransferase, led to activation of the translesion synthesis pathway, thereby allowing the survival in the presence of DNA damage. The DNA damage-induced phosphorylation of Rtt107 and Slx4, which was mutually dependent, was not restored in the absence of Dot1. The antagonistic relationship between Rtt107 and Dot1 was specific for DNA damage-induced phenotypes, whereas the genomic instability caused by loss of Rtt107 was not rescued. These data revealed a multifaceted functional relationship between Rtt107 and Dot1 in the DNA damage response and maintenance of genome integrity.
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