Open AccessHuman chromosome 13 compensates a DNA repair defect in UV-sensitive mouse cells by mouse--human cell hybridization.
Author(s) -
Tada-aki Hori,
Tadahiro Shiomi,
Koki Sato
Publication year - 1983
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.80.18.5655
Subject(s) - biology , complementation , microbiology and biotechnology , somatic cell , mutant , chromosome , dna repair , dna , nucleotide excision repair , gene , karyotype , cell culture , xeroderma pigmentosum , mutation , genetics
A human chromosome responsible for excision repair of UV-induced DNA damage has been identified by studying somatic cell hybrids between an UV-sensitive mutant of mouse lymphoma L5178Y cells and normal human lymphocytes. An autosomal recessive mutant, Q31, of complementation group I is deficient in excision repair of UV-induced DNA damage. Somatic cell hybrids between Q31 and human lymphocytes exhibited the same UV resistance as did parental L5178Y cells. In addition, both the levels of UV-induced unscheduled DNA synthesis and chromosomal sensitivity were recovered from the UV-resistant hybrid clones. Segregation of the hybrid cells gave rise to UV-sensitive clones. The segregation of UV sensitivity was not correlated with the loss of human X chromosome. Karyotype analysis of the segregants gave evidence that a gene on human chromosome 13 compensates for UV hypersensitivity of Q31 mutant.