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Chinese hamster cells meet DNA repair: an entirely acceptable affair
Author(s) -
Thompson Larry H.
Publication year - 1998
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(199807)20:7<589::aid-bies11>3.0.co;2-w
Subject(s) - xeroderma pigmentosum , nucleotide excision repair , dna repair , cockayne syndrome , biology , genetics , complementation , chinese hamster , mutant , chinese hamster ovary cell , postreplication repair , gene , somatic cell , dna , dna damage , microbiology and biotechnology , cell culture
This personal account relates the advent of mutant isolation and other developments in somatic cell genetics that were critical steps toward isolating DNA repair mutants in mammalian cells. The isolation of auxotrophic and temperature‐sensitive mutants in genetically stable Chinese hamster cells during the late 1960s and early 1970s provided a conceptual framework in which to later isolate mutations conferring hypersensitivity to ultraviolet radiation, ionizing radiation, and various chemical mutagens. Complementation group analysis of ultraviolet‐sensitive mutants helped identify multiple genes that overlapped with the groups of cancer‐prone xeroderma pigmentosum, as well as Cockayne syndrome. The first mammalian cell mutants defective in strand‐break repair were also discovered. Subsequent cloning of human genes that corrected CHO‐cell mutations in nucleotide‐excision repair groups 1–6 later led to identifying the key enzymes in the incision steps of this pathway, as well as the CSB protein, which is involved in coupling excision repair and transcription. BioEssays 20 :589–597, 1998. Published 1998 John Wiley & Sons Inc.