ArticleNucleic acids research2008
The effect of sequence context on spontaneous Polzeta-dependent mutagenesis in Saccharomyces cerevisiae.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
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- DNA polymerases ζ and Rev1 mediate error-prone bypass of non-B DNA structures.Nucleic acids research · 2014Article
- Different roles of eukaryotic MutS and MutL complexes in repair of small insertion and deletion loops in yeast.PLoS genetics · 2013Article
- Fragile DNA motifs trigger mutagenesis at distant chromosomal loci in saccharomyces cerevisiae.PLoS genetics · 2013Article
- High levels of transcription stimulate transversions at GC base pairs in yeast.Environmental and molecular mutagenesis · 2013Article
- The dCMP transferase activity of yeast Rev1 is biologically relevant during the bypass of endogenously generated AP sites.DNA repair · 2011Article
- Abasic sites in the transcribed strand of yeast DNA are removed by transcription-coupled nucleotide excision repair.Molecular and cellular biology · 2010Article
- Article
- The mismatch repair system promotes DNA polymerase zeta-dependent translesion synthesis in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- YNK1, the yeast homolog of human metastasis suppressor NM23, is required for repair of UV radiation- and etoposide-induced DNA damage.Mutation research · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
The Polzeta translesion synthesis (TLS) DNA polymerase is responsible for over 50% of spontaneous mutagenesis and virtually all damage-induced mutagenesis in yeast. We previously demonstrated that reversion of the lys2DeltaA746 -1 frameshift allele detects a novel type of +1 frameshift that is accompanied by one or more base substitutions and depends completely on the activity of Polzeta. These 'complex' frameshifts accumulate at two discrete hotspots (HS1 and HS2) in the absence of nucleotide excision repair, and accumulate at a third location (HS3) in the additional absence of the translesion polymerase Poleta. The current study investigates the sequence requirements for accumulation of Polzeta-dependent complex frameshifts at these hotspots. We observed that transposing 13 bp of identity from HS1 or HS3 to a new location within LYS2 was sufficient to recapitulate these hotspots. In addition, altering the sequence immediately upstream of HS2 had no effect on the activity of the hotspot. These data support a model in which misincorporation opposite a lesion precedes and facilitates the selected slippage event. Finally, analysis of nonsense mutation revertants indicates that Polzeta can simultaneously introduce multiple base substitutions in the absence of an accompanying frameshift event.
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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.