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  • 1985-1989  (2)
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  • 1
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The CHO UV-sensitive mutants UV24 and UV135 (complementation groups 3 and 5, respectively) are defective in nucleotide excision repair. After fusing each mutant with human lymphocytes, resistant hybrid clones showing genetic complementation were isolated by repeated exposure to UV radiation. Using a combination of isozyme markers, DNA probes,and cytogenetic methods to analyze the primary hybrids and their subclones, correction of the repair defect was shown to be correlated with the presence of a specific human chromosome in each case. Chromosome 2 corrected UV24, and the gene responsible was designated ERCC3.Line UV135 was corrected by human chromosome 13 and the gene designated ERCC5.The UV-sensitive mouse cell line, Q31, was shown not to complement UV135 and thus appears to be mutated in the same genetic locus (homologous to ERCC5)as UV135. Breakage of complementing chromosomes with retention of the genes correcting repair defects allowed the following provisional assignments: regional localization of ERCC5to 13q14-q34, exclusion of ERCC3from the region of chromosome 2 distal to p23, and relief of the ambiguity of ACPlassignment (2p23 or 2p25) to 2p23 proximal to MDH1.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Somatic cell and molecular genetics 14 (1988), S. 605-612 
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Two mutant lines (US31, US46) of mouse lymphoma cells that are hypersensitive to ultraviolet (UV) radiation were previously found to belong to different complementation groups. The mutants were tested for their ability to complement the six known complementation groups of UV-sensitive Chinese hamster ovary (CHO) cells, which are defective in nucleotide excision repair, as well as a seventh group represented by a V79 mutant. Hybrid cells were produced by fusion with polyethylene glycol and tested in situfor UV resistance. The mouse mutant US46 complemented all CHO mutants except UV61. Therefore, US46 is assigned to the same complementation group as UV61, and it is probably defective in the same locus. The mouse mutant US31 produced UV-resistant hybrid cells in each of the seven crosses, indicating that it forms an eighth complementation group among the rodent mutants. Thus, at least eight genes are likely required to repair UV damage in rodent cells.
    Type of Medium: Electronic Resource
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