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Nature. 1996 Jan 11;379(6561):183-6.

Requirement of mammalian DNA polymerase-beta in base-excision repair.

Author information

1
Sealy Center for Molecular Science, University of Texas Medical Branch, Galveston 77555-1068, USA.

Erratum in

  • Nature 1996 Feb 29;379(6568):848.
  • Nature 1996 Oct 3;383(6599):457.

Abstract

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.

PMID:
8538772
DOI:
10.1038/379183a0
[Indexed for MEDLINE]

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