Document Detail


Gamma-ray mutagenesis studies in a new human-hamster hybrid, A(L)CD59(+/-), which has two human chromosomes 11 but is hemizygous for the CD59 gene.
MedLine Citation:
PMID:  11418068     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Kraemer, S. M., Vannais, D. B., Kronenberg, A., Ueno, A. and Waldren, C. A. Gamma-Ray Mutagenesis Studies in a New Human-Hamster Hybrid, A(L)CD59(+/-), which has Two Human Chromosomes 11 but is Hemizygous for the CD59 Gene. Radiat. Res. 156, 10-19 (2001). We have developed a human-CHO hybrid cell line, named A(L)CD59(+/-), which has two copies of human chromosome 11 but is hemizygous for the CD59 gene and the CD59 cell surface antigen that it encodes. Our previous studies used the A(L) and A(L)C hybrids that respectively contain one or two sets of CHO chromosomes plus a single copy of human chromosome 11. The CD59 gene at 11p13.5 and the CD59 antigen encoded by it are the principal markers used in our mutagenesis studies. The hybrid A(L)CD59(+/-) contains two copies of human chromosome 11, only one of which carries the CD59 gene. The incidence of CD59 (-) mutants (formerly called S1(-)) induced by (137)Cs gamma rays is about fivefold greater in A(L)CD59(+/-) cells than in A(L) cells. Evidence is presented that this increase in mutant yield is due to the increased induction of certain classes of large chromosomal mutations that are lethal to A(L) cells but are tolerated in the A(L)CD59(+/-) hybrid. In addition, significantly more of the CD59 (-) mutants induced by (137)Cs gamma rays in A(L)CD59(+/-) cells display chromosomal instability than in A(L) cells. On the other hand, the yield of gamma-ray-induced CD59 (-) mutants in A(L)CD59(+/-) cells is half that of the A(L)C hybrid, which also tolerates very large mutations but has only one copy of human chromosome 11. We interpret the difference in mutability as evidence that repair processes involving the homologous chromosomes 11 play a role in determining mutant yields. The A(L)CD59(+/-) hybrid provides a useful new tool for quantifying mutagenesis and shedding light on mechanisms of genetic instability and mutagenesis.
Authors:
S M Kraemer; D B Vannais; A Kronenberg; A Ueno; C A Waldren
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Radiation research     Volume:  156     ISSN:  0033-7587     ISO Abbreviation:  Radiat. Res.     Publication Date:  2001 Jul 
Date Detail:
Created Date:  2001-06-21     Completed Date:  2001-07-26     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  0401245     Medline TA:  Radiat Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10-9     Citation Subset:  IM; S    
Affiliation:
Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523, USA. skraemer@lamar.colostate.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD59 / genetics*
CHO Cells
Cell Fusion
Cell Line
Cell Survival / genetics,  radiation effects
Chromosomes, Human, Pair 11* / genetics
Cricetinae
DNA Mutational Analysis
DNA Repair / genetics,  radiation effects
Dose-Response Relationship, Radiation
Fibroblasts / cytology
Gamma Rays*
Gene Dosage
Genetic Markers
Humans
Hybrid Cells / cytology,  radiation effects*
In Situ Hybridization, Fluorescence
Mutagenesis / radiation effects*
Polymerase Chain Reaction
Grant Support
ID/Acronym/Agency:
5T32 CA09236/CA/NCI NIH HHS; CA36447/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD59; 0/Genetic Markers
Investigator
Investigator/Affiliation:
A Chatterjee / U CA, Berkeley

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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