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Evidence for mutagenic repair in V79 cell mutant with aphidicolin-resistant DNA polymerase-α

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Somatic Cell and Molecular Genetics

Abstract

An aphidicolin-resistant (aphr) mutant of Chinese hamster V79 cells, aphr-4-2, is shown to be slow-growing, sensitive to ultraviolet (UV) irradiation, hypermutable for spontaneous and UV-induced mutations, and known to contain an aphr mutant DNA polymerase-α, with a 10-fold reduction in the Km for dCTP but not for dATP. We show here that the mutant had a normal repair replication measured by unscheduled DNA synthesis assay. The mutant was specifically sensitive and hypermutable to UV and N-methyl-N′-nitro-N-nitrosoguanidine, but it had normal sensitivity to ionizing radiation and dimethyl sulfate. Unlike the V79 (wt) cells, the mutant exhibited further enhancement in the already elevated mutability following UV and conditioned medium treatment. The mutant characteristic is explained by the presence of an error-prone long-patch excision repair synthesis. The association in the mutant properties—an aphr DNA polymerase-α, UV sensitivity, and hypermutability to UV-induced mutation—provides the genetic evidence that DNA polymerase-α is likely to be involved in UV-induced DNA repair synthesis.

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Author notes

  1. Philip K. Liu

    Present address: The Joseph Gottstein Memorial Cancer Research Laboratory, Department of Pathology SM-30, University of Washington, 98195, Seattle, Washington

Authors and Affiliations

  1. Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University, 48824, East Lansing, Michigan

    Philip K. Liu, Chia -cheng Chang & James E. Trosko

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  1. Philip K. Liu
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  2. Chia -cheng Chang
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  3. James E. Trosko
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Liu, P.K., Chang, C.c. & Trosko, J.E. Evidence for mutagenic repair in V79 cell mutant with aphidicolin-resistant DNA polymerase-α. Somat Cell Mol Genet 10, 235–245 (1984). https://doi.org/10.1007/BF01535246

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  • DOI: https://doi.org/10.1007/BF01535246

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