Scc1/Rad21/Mcd1 is required for sister chromatid cohesion and kinetochore function in vertebrate cells

被引:233
作者
Sonoda, E
Matsusaka, T
Morrison, C
Vagnarelli, P
Hoshi, O
Ushiki, T
Nojima, K
Fukagawa, T
Waizenegger, IC
Peters, JM
Earnshaw, WC
Takeda, S [1 ]
机构
[1] Kyoto Univ, Fac Med, JST, CREST Res Project,Sakyo Ku, Kyoto 6068501, Japan
[2] Kyoto Univ, Grad Sch Biostudies, Dept Gene Mech, Sakyo Ku, Kyoto 6068502, Japan
[3] Univ Edinburgh, Inst Cell & Mol Biol, Wellcome Trust Ctr Cell Biol, Edinburgh EH9 3JR, Midlothian, Scotland
[4] Niigata Univ, Fac Med, Dept Anat & Histol, Niigata 9518510, Japan
[5] Grad Univ Adv Studies, JST, PRESTO, Shizuoka 4118540, Japan
[6] Res Inst Mol Pathol, A-1030 Vienna, Austria
基金
英国惠康基金;
关键词
D O I
10.1016/S1534-5807(01)00088-0
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Proteolytic cleavage of the cohesin subunit Scc1 is a consistent feature of anaphase onset, although temporal differences exist between eukaryotes in cohesin loss from chromosome arms, as distinct from centromeres. We describe the effects of genetic deletion of Scc1 in chicken DT40 cells. Scc1 loss caused premature sister chromatid separation but did not disrupt chromosome condensation. Scc1 mutants showed defective repair of spontaneous and induced DNA damage. Scc1-deficient cells frequently failed to complete metaphase chromosome alignment and showed chromosome segregation defects, suggesting aberrant kinetochore function. Notably, the chromosome passenger INCENP did not localize normally to centromeres, while the constitutive kinetochore proteins CENP-C and CENP-H behaved normally. These results suggest a role for Scc1 in mitotic regulation, along with cohesion.
引用
收藏
页码:759 / 770
页数:12
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