ArticleMolecular and cellular biology1997
Hypermutability of homonucleotide runs in mismatch repair and DNA polymerase proofreading yeast mutants.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers.
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197 citing papers in PubMed, 313 citations in OpenAlex.
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- Site directed mutagenesis reveals functional importance of conserved amino acid residues within the N-terminal domain of Dpb2 in budding yeast.Archives of microbiology · 2024Article
- Effects of PCNA Stability on the Formation of Mutations.International journal of molecular sciences · 2024Article
- MutLα suppresses error-prone DNA mismatch repair and preferentially protects noncoding DNA from mutations.The Journal of biological chemistry · 2024Article
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- Deficiency in homologous recombination is associated with changes in cell cycling and morphology in Saccharomyces cerevisiae.Experimental cell research · 2023Article
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- Rad27 and Exo1 function in different excision pathways for mismatch repair in Saccharomyces cerevisiae.Nature communications · 2021Article
137 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homonucleotide runs in coding sequences are hot spots for frameshift mutations and potential sources of genetic changes leading to cancer in humans having a mismatch repair defect. We examined frameshift mutations in homonucleotide runs of deoxyadenosines ranging from 4 to 14 bases at the same position in the LYS2 gene of the yeast Saccharomyces cerevisiae. In the msh2 mismatch repair mutant, runs of 9 to 14 deoxyadenosines are 1,700-fold to 51,000-fold, respectively, more mutable for single-nucleotide deletions than are runs of 4 deoxyadenosines. These frameshift mutations can account for up to 99% of all forward mutations inactivating the 4-kb LYS2 gene. Based on results with single and double mutations of the POL2 and MSH2 genes, both DNA polymerase epsilon proofreading and mismatch repair are efficient for short runs while only the mismatch repair system prevents frameshift mutations in runs of > or = 8 nucleotides. Therefore, coding sequences containing long homonucleotide runs are likely to be at risk for mutational inactivation in cells lacking mismatch repair capability.
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