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YeastRAD14 and human xeroderma pigmentosum group A DNA-repair genes encode homologous proteins

Nature volume 355, pages 555–558 (1992)Cite this article

Abstract

XERODERMA pigmentosum (XP), a human autosomal recessive disorder, is characterized by extreme sensitivity to sunlight and high incidence of skin cancers. XP cells are defective in the incision step of excision repair of DNA damaged by ultraviolet light. Cell fusion studies have defined seven XP complementation groups, XP-A to XP-G (refs 1,2). Similar genetic complexity of excision repair is observed in the yeast Saccharomyces cerevisiae. Mutations in any one of five yeast genes, RAD1, RAD2, RAD3, RAD4, and RAD10, cause a total defect in incision and an extreme sensitivity to ultraviolet light3. Here we report the characterization of the yeast RAD14 gene. The available radl4 point mutant is only moderately ultraviolet-sensitive, and it performs a substantial amount of incision of damaged DNA4,5. Our studies with the radl4 deletion (A) mutation indicate an absolute requirement of RAD14 in incision. RAD14 encodes a highly hydrophilic protein of 247 amino acids containing zinc-finger motifs, and it is similar to the protein encoded by the human XPAC gene that complements XP group A cell lines6.

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Authors and Affiliations

  1. Department of Biophysics, University of Rochester School of Medicine, 601 Elmwood Avenue, Rochester, New York, 14642-8408, USA

    Michael Bankmann & Louise Prakash

  2. Department of Biology, University of Rochester, River Campus Station, Rochester, New York, 14627, USA

    Satya Prakash

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  1. Michael Bankmann
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  2. Louise Prakash
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  3. Satya Prakash
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Bankmann, M., Prakash, L. & Prakash, S. YeastRAD14 and human xeroderma pigmentosum group A DNA-repair genes encode homologous proteins. Nature 355, 555–558 (1992). https://doi.org/10.1038/355555a0

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