Critical role for chicken Rad17 and Rad9 in the cellular response to DNA damage and stalled DNA replication

被引：37

作者：

Kobayashi, M

Hirano, A

Kumano, T

Xiang, SL

Mihara, K

Haseda, Y

Matsui, O

Shimizu, H

Yamamoto, K ^{[1
]}

机构：

[1] Kanazawa Univ, Canc Res Inst, Dept Mol Pathol, Kanazawa, Ishikawa 9200934, Japan

[2] Kanazawa Univ, Canc Res Inst, Ctr Dev Mol Target Drugs, Kanazawa, Ishikawa 9200934, Japan

[3] Kanazawa Univ, Grad Sch Med, Dept Radiol, Kanazawa, Ishikawa 9200934, Japan

来源：

GENES TO CELLS | 2004年 / 9卷 / 04期

关键词：

D O I：

10.1111/j.1356-9597.2004.00728.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The Rad17-replication factor C (Rad17-RFC) and Rad9-Rad1-Hus1 complexes are thought to function in the early phase of cell-cycle checkpoint control as sensors for genome damage and genome replication errors. However, genetic analysis of the functions of these complexes in vertebrates is complicated by the lethality of these gene disruptions in embryonic mouse cells. We disrupted the Rad17 and Rad9 loci by gene targeting in the chicken B lymphocyte line DT40. Rad17(-/-) and Rad9(-/-) DT40 cells are viable, and are highly sensitive to UV irradiation, alkylating agents, and DNA replication inhibitors, such as hydroxyurea. We further found that Rad17(-/-) and Rad9(-/-) but not ATM(-/-) cells are defective in S-phase DNA damage checkpoint controls and in the cellular response to stalled DNA replication. These results indicate a critical role for chicken Rad17 and Rad9 in the cellular response to stalled DNA replication and DNA damage.

引用

页码：291 / 303

页数：13

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