YEAST RAD14 AND HUMAN XERODERMA-PIGMENTOSUM GROUP-A DNA-REPAIR GENES ENCODE HOMOLOGOUS PROTEINS
YEAST RAD14 AND HUMAN XERODERMA-PIGMENTOSUM GROUP-A DNA-REPAIR GENES ENCODE HOMOLOGOUS PROTEINS
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DOI：
10.1038/355555a0
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发表时间：
1992-02-06
期刊：
影响因子：
64.8
通讯作者：
PRAKASH, S
中科院分区：
文献类型：
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作者：
BANKMANN, M;PRAKASH, L;PRAKASH, S
着色性干皮病是一种常染色体隐性遗传病，对阳光极度敏感，皮肤癌发病率高。XP细胞在紫外线损伤的DNA的切除修复的切割步骤中有缺陷。细胞融合研究已经确定了七个XP互补组，XP-A至XP-G（参考文献1，2）。在酵母酿酒酵母中观察到类似的切除修复遗传复杂性。5种酵母基因中的任何一种突变，即RAD 1、RAD 2、RAD 3、RAD 4和RAD 10，都会导致切口的完全缺陷和对紫外线的极端敏感性。在这里，我们报告的酵母RAD 14基因的特性。可用的rad 14点突变体仅具有中等的紫外线敏感性，并且它对受损的DNA进行了大量的切割4，5。我们对rad 14缺失（DELTA）突变的研究表明，在切口中绝对需要RAD 14。RAD 14编码一种含有锌指基序的247个氨基酸的高度亲水性蛋白质，并且它类似于由人XPAC基因编码的补充XP A组细胞系6的蛋白质。
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 light 3. Here we report the characterization of the yeast RAD14 gene. The available rad14 point mutant is only moderately ultraviolet-sensitive, and it performs a substantial amount of incision of damaged DNA 4,5. Our studies with the rad14 deletion (DELTA) 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 lines 6.