Human chromosome 15 confers partial complementation of phenotypes to xeroderma pigmentosum group F cells.
Microcell-mediated transfer of a single human chromosome from repair-proficient human cells to genetic complementation group F cells from the hereditary disease xeroderma pigmentosum (XP) results in partial complementation of repair-defective phenotypes. The complementing chromosome was identified by cytogenetic and molecular analysis as human chromosome 15. Transfer of this chromosome to XP-F cells restores approximately 20% of the resistance of wild-type cells to killing by UV radiation or by the UV-mimetic chemical 4-nitroquinoline-1-oxide (4NQO), as well as partial repair synthesis of DNA measured as unscheduled DNA synthesis. Additionally, complemented XP-F cells have an enhanced capacity for reactivation of the plasmid-borne E. coli cat gene following its inactivation by UV radiation. Phenotypic complementation of XP cells by chromosome 15 is specific to genetic complementation group F; no effect on the UV sensitivity of XP-A, XP-C, or XP-D cells was detected. The observation that phenotypic complementation is partial is open to several interpretations and does not allow the definitive conclusion that the XP-F locus is carried on chromosome 15.
Saxon
P J
PJ
Department of Pathology, Stanford University School of Medicine, CA 94305.
Schultz
R A
RA
Stanbridge
E J
EJ
Friedberg
E C
EC
D002455:Cell Division; D002871:Chromosome Banding; D002874:Chromosome Mapping; D002884:Chromosomes, Human, Pair 15; D004249:DNA Damage; D004260:DNA Repair; D005816:Genetic Complementation Test; D006801:Humans; D010641:Phenotype; D014983:Xeroderma Pigmentosum / Q000235:genetics*