Human chromosome 15 confers partial complementation of phenotypes to xeroderma pigmentosum group F cells

P. J. Saxon, R. A. Schultz, E. J. Stanbridge, E. C. Friedberg

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

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 ~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 plasmic-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.

Original languageEnglish (US)
Pages (from-to)474-485
Number of pages12
JournalAmerican Journal of Human Genetics
Volume44
Issue number4
StatePublished - 1989

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

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