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 Citations (Scopus)

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

Fingerprint

Chromosomes, Human, Pair 15
Xeroderma Pigmentosum
Human Chromosomes
Phenotype
Chromosomes
4-Nitroquinoline-1-oxide
Radiation
Inborn Genetic Diseases
Somatostatin-Secreting Cells
Cytogenetic Analysis
DNA Repair
Cats
Escherichia coli
DNA

ASJC Scopus subject areas

  • Genetics

Cite this

Human chromosome 15 confers partial complementation of phenotypes to xeroderma pigmentosum group F cells. / Saxon, P. J.; Schultz, R. A.; Stanbridge, E. J.; Friedberg, E. C.

In: American Journal of Human Genetics, Vol. 44, No. 4, 1989, p. 474-485.

Research output: Contribution to journalArticle

@article{caa0425abe564196bf42a622f8016d46,
title = "Human chromosome 15 confers partial complementation of phenotypes to xeroderma pigmentosum group F cells",
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.",
author = "Saxon, {P. J.} and Schultz, {R. A.} and Stanbridge, {E. J.} and Friedberg, {E. C.}",
year = "1989",
language = "English (US)",
volume = "44",
pages = "474--485",
journal = "American Journal of Human Genetics",
issn = "0002-9297",
publisher = "Cell Press",
number = "4",

}

TY - JOUR

T1 - Human chromosome 15 confers partial complementation of phenotypes to xeroderma pigmentosum group F cells

AU - Saxon, P. J.

AU - Schultz, R. A.

AU - Stanbridge, E. J.

AU - Friedberg, E. C.

PY - 1989

Y1 - 1989

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0024600323&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024600323&partnerID=8YFLogxK

M3 - Article

VL - 44

SP - 474

EP - 485

JO - American Journal of Human Genetics

JF - American Journal of Human Genetics

SN - 0002-9297

IS - 4

ER -