Oncotarget

Research Papers:

PTEN regulates spindle assembly checkpoint timing through MAD1 in interphase

Yu Liu, Xiao Du, Shuting Zhang, Yang Liu, Qiaoling Zhang, Qi Yin, Michael A. McNutt and Yuxin Yin _

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Oncotarget. 2017; 8:98040-98050. https://doi.org/10.18632/oncotarget.20532

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Abstract

Yu Liu1,*, Xiao Du1,*, Shuting Zhang1, Yang Liu1, Qiaoling Zhang1, Qi Yin1, Michael A. McNutt1 and Yuxin Yin1

1Institute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China

*These authors have contributed equally to this work

Correspondence to:

Yuxin Yin, email: [email protected]

Keywords: PTEN; MAD1; spindle assembly checkpoint; mitosis; genome stability

Received: November 25, 2016    Accepted: August 04, 2017    Published: August 24, 2017

ABSTRACT

The spindle assembly checkpoint (SAC) restrains anaphase progression to ensure all chromosomes attach properly to the spindle. Although SAC timing has been extensively investigated in mitosis, its mechanism of regulation in interphase is unclear. We report that PTEN functions as a crucial activator of SAC timing and protects chromosome segregation under both spindle poison treated and untreated conditions. We show that PTEN physically interacts with MAD1 and promotes its dimerization and localization in the nuclear pore. Consequently, PTEN is important for the formation of the mitotic checkpoint complex (MCC) in interphase. We propose PTEN/MAD1 signaling is essential for maintenance of SAC timing and chromosome integrity.


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