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Repair-Deficient Xeroderma Pigmentosum Cells Made UV Light Resistant by Fusion with X-Ray-Inactivated Chinese Hamster Cells
Author(s) -
Deneb Karentz,
James E. Cleaver
Publication year - 1986
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.6.10.3428-3432.1986
Subject(s) - xeroderma pigmentosum , chinese hamster ovary cell , biology , microbiology and biotechnology , chinese hamster , dna repair , nucleotide excision repair , dna , cell culture , ultraviolet light , cell fusion , ataxia telangiectasia , genetics , dna damage , chemistry , photochemistry
Xeroderma pigmentosum (XP) is an autosomal recessive human disease, characterized by an extreme sensitivity to sunlight, caused by the inability of cells to repair UV light-induced damage to DNA. Cell fusion was used to transfer fragments of Chinese hamster ovary (CHO) chromosomes into XP cells. The hybrid cells exhibited UV resistance and DNA repair characteristics comparable to those expressed by CHO cells, and their DNA had greater homology with CHO DNA than did the DNA from XP cells. Control experiments consisted of fusion of irradiated and unirradiated XP cells and repeated exposure of unfused XP cells to UV doses used for hybrid selection. These treatments did not result in an increase in UV resistance, repair capability, or homology with CHO DNA. The hybrid cell lines do not, therefore, appear to be XP revertants. The establishment of these stable hybrid cell lines is an initial step toward identifying and cloning CHO DNA repair genes that complement the XP defect in human cells. The method should also be applicable to cloning genes for other diseases, such as ataxia-telangiectasia and Fanconi's anemia.

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