Down-regulation of PARP-1, but not of Ku80 or DNA-PKcs, results in higher gene targeting efficiency

被引：17
|
作者：
Domínguez-Bendala, J
Masutani, M
McWhir, J [1 ]
机构：
[1] Roslin Inst, Div Gene Express & Dev, Roslin EH25 9PS, Midlothian, Scotland
[2] Univ Miami, Diabet Res Inst, Miami, FL 33136 USA
[3] Natl Canc Ctr, ADP Ribosylat Oncol Project, Chuo Ku, Tokyo 1040045, Japan
来源：
CELL BIOLOGY INTERNATIONAL | 2006年 / 30卷 / 04期
基金：
英国生物技术与生命科学研究理事会;
关键词：
homologous recombination; PARP-1; Ku80; DNA-PK; gene targeting; ES cells;
D O I：
10.1016/j.cellbi.2005.12.005
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The viability of non-homologous end-joining (NHEJ)-defective mice suggests that homologous recombination (HR) might take over its role in DNA repair. To test this hypothesis, we examined gene targeting frequencies (TF) in DNA-PKcs, Ku80 and poly(ADP-ribose) polymerase (PARP-1) nullizygous cells. We observed a 3-fold TF increase in PARP-1 knockout embryonic stem (ES) cells, which is consistent with the predicted role of PARP-I as a switch between HR and NHEJ. To a lesser extent, such effect could be reproduced upon chemical inhibition of PARP-1. However, TF was not enhanced in Ku80- or DNA-PKcs-defective cells. Our study also suggests an unexpected involvement of DNA-PKcs in HR. (c) 2006 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码：389 / 393
页数：5
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