Human chromosome 9 can complement UV sensitivity of xeroderma pigmentosum group A cells.
A single human chromosome derived from normal human fibroblasts and tagged with the G418 resistance gene was transferred into SV40-transformed xeroderma pigmentosum group A (XP-A) cells via microcell fusion. When chromosome 1 or 12 was transferred, UV sensitivity of microcell hybrid cells was not changed. By contrast, after transferring chromosome 9, 7 of 11 recipient clones were as UV-resistant as normal human cells. Four other clones were still as UV-sensitive as the parental XP-A cells. Southern hybridization analysis using a polymorphic probe, pEKZ19.3, which is homologous to a sequence of the D9S17 locus on chromosome 9, has confirmed that at least a part of normal human chromosome 9 was transferred into the recipient clones. However, amounts of UV-induced unscheduled DNA synthesis in the UV-resistant clones were only one-third of those in normal human cells. These results indicate that a gene on chromosome 9 can confer complementation of high UV sensitivity of XP-A cells although it is still possible that 2 or more genes might be involved in the defective-repair phenotypes of XP-A.
Ishizaki
K
K
Radiation Biology Center, Kyoto University, Japan.
Oshimura
M
M
Sasaki
M S
MS
Nakamura
Y
Y
Ikenaga
M
M
D015139:Blotting, Southern; D002470:Cell Survival; D002899:Chromosomes, Human, Pair 9; D004247:DNA / Q000096:biosynthesis / Q000528:radiation effects; D004260:DNA Repair / Q000235:genetics; D006801:Humans; D006822:Hybrid Cells; D009154:Mutation; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000235:genetics*
D004247:DNA