| First Author | Sobol RW | Year | 1996 |
| Journal | Nature | Volume | 379 |
| Issue | 6561 | Pages | 183-6 |
| PubMed ID | 8538772 | Mgi Jnum | J:30634 |
| Mgi Id | MGI:78137 | Doi | 10.1038/379183a0 |
| Citation | Sobol RW, et al. (1996) Requirement of mammalian DNA polymerase-beta in base-excision repair. Nature 379(6561):183-6 |
| abstractText | Synthesis of DNA by DNA polymerase-beta is distributive on single-stranded DNA templates, but short DNA gaps with a 5' PO4 in the gap are filled processively to completion. In vitro studies have suggested a role of beta-polymerase in different types of DNA repair. However, the significance of these studies to the in vivo role of beta-polymerase has remained unclear. Because genetic studies are essential for determining the physiological role of a gene, we established embryonic fibroblast cell lines homozygous for a deletion mutation in the gene encoding DNA polymerase-beta. Extracts from these cell lines were found to be defective in uracil-initiated base-excision repair. The beta-polymerase-deleted cells are normal in viability and growth characteristics, although they exhibit increased sensitivity to monofunctional DNA-alkylating agents, but not to other DNA-damaging agents. Both the deficiency in base-excision repair and hypersensitivity to DNA-alkylating agents are rescued following stable transfection with a wild-type beta-polymerase minitransgene. These studies demonstrate that beta-polymerase functions specifically in base-excision repair in vivo. |
