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 language||English (US)|
|Number of pages||12|
|State||Published - 2009|
Bibliographical noteFunding Information:
Acknowledgments This work was supported by a grant from the National Institutes of Neurological Disorders and Stroke. We thank Yuri Nesmelov for translating portions of the Genetika references.
- HMG protein