ArticleCurrent genetics2009
Suppression of a DNA polymerase delta mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae.
Article in Current genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Hmo1: A versatile member of the high mobility group box family of chromosomal architecture proteins.World journal of biological chemistry · 2024Review
- Participation of the HIM1 gene of yeast Saccharomyces cerevisiae in the error-free branch of post-replicative repair and role Polη in him1-dependent mutagenesis.Current genetics · 2021Article
- Yeast high mobility group protein HMO1 stabilizes chromatin and is evicted during repair of DNA double strand breaks.Nucleic acids research · 2015Article
- DNA bending facilitates the error-free DNA damage tolerance pathway and upholds genome integrity.The EMBO journal · 2014Article
- Hmo1 directs pre-initiation complex assembly to an appropriate site on its target gene promoters by masking a nucleosome-free region.Nucleic acids research · 2011Article
- Maintaining genome stability at the replication fork.Nature reviews. Molecular cell biology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deletion of the gene encoding the high mobility group protein Hmo1 suppresses the growth retardation of the DNA pol delta mutation, pol3-14, at the restrictive temperature. pol3-14 mutant cells undergo cell cycle arrest, and hmo1Delta alleviates the arrest permitting continual division of the double mutant. Bypass of cell cycle control occurs with an increased rate of mutation. Both pol3-14 and hmo1Delta are mutators and their combination provokes a synergistic rate of CAN1 mutations. RAD18 controls branches of DNA repair pathways and its deletion also suppresses pol3 mutations. Comparing hmo1Delta and rad18Delta suppression of pol3-14 shows that while both require the presence of RAD52-mediated repair, their suppression is independent in that both can suppress in the presence of the other. We conclude that hmo1Delta suppression of pol3-14 occurs by a mechanism whereby normal controls on DNA integrity are breached and lesions flow into RAD52-mediated repair and error-prone pathways.
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Registered trials
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