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Aneuploidy, an abnormal chromosome set, can ensue from failure of the spindle checkpoint, the safeguard mechanism that halts anaphase onset until mitotic spindle assembly. Inefficiency of cells to maintain the normal chromosome set across cell generations has been linked to tumorigenesis and senescence. Here we show that oxidative stress overrides the spindle checkpoint mechanism. Oxidant challenge of checkpoint-arrested cells led to proteolysis of the anaphase inhibitor securin and mitotic cyclins. This appeared consequent to loss of cyclin B-cdk1 activity caused by oxidant-induced reversal of cdk1 inhibitory phosphorylation. These observations may provide a link between aneuploidy occurrence and oxidative stress.

Original publication

DOI

10.4161/cc.6.5.3934

Type

Journal article

Journal

Cell Cycle

Publication Date

01/03/2007

Volume

6

Pages

576 - 579

Keywords

Cell Cycle, Cyclin B1, Cyclin-Dependent Kinases, HeLa Cells, Humans, Oxidants, Oxidative Stress, Spindle Apparatus