Open AccessRETRACTED: Involvement of Hus1 in the chain elongation step of DNA replication after exposure to camptothecin or ionizing radiation
Author(s) -
Xiang Wang,
Jun Guan,
B. Y. Hu,
Robert S. Weiss,
George Iliakis,
Ya Wang
Publication year - 2004
Publication title -
nucleic acids research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 9.008
H-Index - 537
eISSN - 1362-4954
pISSN - 0305-1048
DOI - 10.1093/nar/gkh243
Subject(s) - g2 m dna damage checkpoint , dna damage , camptothecin , biology , chek1 , proliferating cell nuclear antigen , dna replication , elongation , dna , microbiology and biotechnology , cell cycle , cell cycle checkpoint , biochemistry , cell , materials science , ultimate tensile strength , metallurgy
DNA damage-induced S phase (S) checkpoint includes inhibition of both replicon initiation and chain elongation. The precise mechanism for controlling the two processes remains unclear. In this study, we showed that Hus1-deficient mouse cells had an impaired S checkpoint after exposure to DNA strand break-inducing agents such as camptothecin (CPT) (>or=1.0 micro M), or ionizing radiation (IR) (>or=15 Gy). The Hus1-dependent S checkpoint contributes to cell resistance to CPT. This impaired S checkpoint induced by CPT or IR in Hus1-deficient cells reflected mainly the chain elongation step of DNA replication and was correlated with the reduction of dissociation of PCNA from DNA replication foci. Although Hus1 is required for Rad9 phosphorylation following exposure of cells to CPT or IR, Hus1-deficient cells showed normal activation of ATR/CHK1 and ATM kinases at doses where the checkpoint defects were manifested, suggesting that Hus1 is not a component of the sensor system for activating these pathways in S checkpoint induced by CPT or IR.