The molecular genetics of the incision step in the DNA excision repair process.
The molecular genetics of the incision step in the DNA excision repair process.
复制标题
DNA 切除修复过程中切口步骤的分子遗传学。
DOI:
10.1080/09553008814551751
复制
发表时间:
1988
影响因子:
2.6
通讯作者:
Rubin,JS
中科院分区:
文献类型:
--
作者:
Rubin,JS
This review describes the evolution of research into the genetic basis of how different organisms use the process of excision repair to recognize and remove lesions from their cellular DNA. One particular aspect of excision repair, DNA incision, and how it is controlled at the genetic level in bacteriophage, bacteria,S. cerevisae,D. melanogaster, rodent cells and humans is examined. In phage T4, DNA is incised by a DNA glycosylase-AP endonuclease that is coded for by thedenVgene. InE. coli, the products of three genes,uvrA,uvrBanduvrC, are required to form the UVRABC excinuclease that cleaves DNA and releases a fragment 12–13 nucleotides long containing the site of damage. InS. cerevisiae, genes complementing five mutants of theRAD3epistasis group,rad1,rad2,rad3,rad4andrad10have been cloned and analyzed. Rodent cells sensitive to a variety of mutagenic agents and deficient in excision repair are being used in molecular studies to identify and clone human repair genes (e.g.ERCC1) capable of complementing mammalian repair defects. Most studies of the human system, however, have been done with cells isolated from patients suffering from the repair defective, cancer-prone disorder, xeroderma pigmentosum, and these cells are now beginning to be characterized at the molecular level. Studies such as these that provide a greater understanding of the genetic basis of DNA repair should also offer new insights into other cellular processes, including genetic recombination, differentiation, mutagenesis, carcinogenesis and aging.