期刊
GENES & DEVELOPMENT
卷 17, 期 1, 页码 77-87出版社
COLD SPRING HARBOR LAB PRESS
DOI: 10.1101/gad.1048303
关键词
DNA polymerase; thymine glycol; translesion DNA synthesis; Pol zeta as an extender; error-free translesion DNA synthesis by Pol zeta yeast
资金
- NATIONAL CANCER INSTITUTE [R37CA041261, R01CA041261] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES006676] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA041261, R37 CA041261, CA41261] Funding Source: Medline
- NIEHS NIH HHS [P30 ES006676, P30-ES06676] Funding Source: Medline
- NIGMS NIH HHS [GM19261] Funding Source: Medline
DNA polymerase zeta (Pole) promotes the mutagenic bypass of DNA lesions in eukaryotes. Genetic studies in Saccharomyces cerevisiae have indicated that relative to the contribution of other pathways, Polzeta makes only a modest contribution to lesion bypass. Intriguingly, however, disruption of the REV3 gene, which encodes the catalytic subunit of Polzeta causes early embryonic lethality in mice. Here, we present genetic and biochemical evidence for the requirement of yeast Polzeta for predominantly error-free replication past thymine glycol (Tg), a DNA lesion formed frequently by free radical attack. These results raise the possibility that, as in yeast, in higher eukaryotes also, Polzeta makes a major contribution to the replicative bypass of Tgs as well as other lesions that block synthesis by replicative DNA polymerases. Such a preeminent role of Polzeta in lesion bypass would ensure that rapid cell divisions continue unabated during early embryonic development, thereby minimizing the generation of DNA strand breaks, chromosome aberrations, and the ensuing apoptotic response.
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