Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype

Fukao, T, Chen, P, Ren, J, Kaneko, H, Zhang, GX, Kondo, M, Yamamoto, K, Furuichi, Y, Takeda, S, Kondo, N and Lavin, MF (2004) Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype. Oncogene, 23 8: 1498-1506. doi:10.1038/sj.onc.1207276


Author Fukao, T
Chen, P
Ren, J
Kaneko, H
Zhang, GX
Kondo, M
Yamamoto, K
Furuichi, Y
Takeda, S
Kondo, N
Lavin, MF
Title Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype
Journal name Oncogene   Check publisher's open access policy
ISSN 0950-9232
Publication date 2004-01-01
Sub-type Article (original research)
DOI 10.1038/sj.onc.1207276
Volume 23
Issue 8
Start page 1498
End page 1506
Total pages 9
Editor E. P. Reddy
J. Jenkins
Place of publication London, U.K.
Publisher Nature Publishing Group
Collection year 2004
Language eng
Subject C1
321204 Mental Health
730204 Child health
Abstract Bloom syndrome and ataxia-telangiectasia are autosomal recessive human disorders characterized by immunodeficiency, genome instability and predisposition to develop cancer. Recent data reveal that the products of these two genes, BLM and ATM, interact and function together in recognizing abnormal DNA structures. To investigate the function of these two molecules in DNA damage recognition, we generated double knockouts of ATM(-/-) BLM-/- in the DT40 chicken B-lymphocyte cell line. The double mutant cells were viable and exhibited a variety of characteristics of both ATM(-/-) and BLM-/- cells. There was no evidence for exacerbation of either phenotype; however, the more extreme radiosensitivity seen in ATM(-/-) and the elevated sister chromatid exchange seen in BLM-/- cells were retained in the double mutants. These results suggest that ATM and BLM have largely distinct roles in recognizing different forms of damage in DNA, but are also compatible with partially overlapping functions in recognizing breaks in radiation-damaged DNA.
Keyword Biochemistry & Molecular Biology
Oncology
Cell Biology
Genetics & Heredity
Ataxia-telangiectasia
Bloom Syndrome
Dna Damage
Dt40 Cells
Gene Disruption
Blooms-syndrome Gene
Double-strand Breaks
Ionizing-radiation
Dna-damage
Dependent Phosphorylation
Recombinational Repair
Genomic Instability
Syndrome Protein
S-phase
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
2005 Higher Education Research Data Collection
School of Medicine Publications
 
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Created: Wed, 15 Aug 2007, 13:24:06 EST