ArticleMolecular and cellular biology2005
Inactivation of Ku-mediated end joining suppresses mec1Delta lethality by depleting the ribonucleotide reductase inhibitor Sml1 through a pathway controlled by Tel1 kinase and the Mre11 complex.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Chromatin assembly factor-1 preserves genome stability inCell stress · 2023Article
- Replisome function during replicative stress is modulated by histone h3 lysine 56 acetylation through Ctf4.Genetics · 2015Article
- Telomere length kinetics assay (TELKA) sorts the telomere length maintenance (tlm) mutants into functional groups.Nucleic acids research · 2014Article
- TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability.The Journal of cell biology · 2014Article
- Mec1p associates with functionally compromised telomeres.Chromosoma · 2012Article
- dNTP pools determine fork progression and origin usage under replication stress.The EMBO journal · 2012Article
- Differential regulation of the cellular response to DNA double-strand breaks in G1.Molecular cell · 2008Article
- Mdt1 facilitates efficient repair of blocked DNA double-strand breaks and recombinational maintenance of telomeres.Molecular and cellular biology · 2007Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
RAD53 and MEC1 are essential Saccharomyces cerevisiae genes required for the DNA replication and DNA damage checkpoint responses. Their lethality can be suppressed by increasing the intracellular pool of deoxynucleotide triphosphates. We report that deletion of YKU70 or YKU80 suppresses mec1Delta, but not rad53Delta, lethality. We show that suppression of mec1Delta lethality is not due to Ku--associated telomeric defects but rather results from the inability of Ku- cells to efficiently repair DNA double strand breaks by nonhomologous end joining. Consistent with these results, mec1Delta lethality is also suppressed by lif1Delta, which like yku70Delta and yku80Delta, prevents nonhomologous end joining. The viability of yku70Delta mec1Delta and yku80Delta mec1Delta cells depends on the ATM-related Tel1 kinase, the Mre11-Rad50-Xrs2 complex, and the DNA damage checkpoint protein Rad9. We further report that this Mec1-independent pathway converges with the Rad53/Dun1-regulated checkpoint kinase cascade and leads to the degradation of the ribonucleotide reductase inhibitor Sml1.
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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.