Suppression of a DNA polymerase δ mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae

Haeyoung Kim, Dennis M. Livingston

Research output: Contribution to journalReview article

5 Citations (Scopus)

Abstract

The deletion of the gene encoding the high mobility group protein Hmo1 suppresses the growth retardation of the DNA pol δ mutation, pol3-14, at the restrictive temperature. pol3-14 mutant cells undergo cell cycle arrest, and hmo1Δ 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 hmo1Δ 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 hmo1Δ and rad18Δ 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 hmo1Δ 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.

Original languageEnglish (US)
Pages (from-to)127-138
Number of pages12
JournalCurrent Genetics
Volume55
Issue number2
DOIs
StatePublished - Feb 12 2009

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High Mobility Group Proteins
Mutation Rate
DNA-Directed DNA Polymerase
Cell Cycle Checkpoints
Saccharomyces cerevisiae
Mutation
DNA
Gene Deletion
DNA Repair
Temperature
Growth

Keywords

  • HMG protein
  • Hmo1
  • POL3
  • RAD18
  • RAD52

Cite this

Suppression of a DNA polymerase δ mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae. / Kim, Haeyoung; Livingston, Dennis M.

In: Current Genetics, Vol. 55, No. 2, 12.02.2009, p. 127-138.

Research output: Contribution to journalReview article

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N2 - The deletion of the gene encoding the high mobility group protein Hmo1 suppresses the growth retardation of the DNA pol δ mutation, pol3-14, at the restrictive temperature. pol3-14 mutant cells undergo cell cycle arrest, and hmo1Δ 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 hmo1Δ 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 hmo1Δ and rad18Δ 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 hmo1Δ 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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