Involvement of CNOT3 in mitotic progression through inhibition of MAD1 expression

Biochemical and Biophysical Research Communications
Akinori TakahashiTadashi Yamamoto

Abstract

The stability of mRNA influences the dynamics of gene expression. The CCR4-NOT complex, the major deadenylase in mammalian cells, shortens the mRNA poly(A) tail and contributes to the destabilization of mRNAs. The CCR4-NOT complex plays pivotal roles in various physiological functions, including cell proliferation, apoptosis, and metabolism. Here, we show that CNOT3, a subunit of the CCR4-NOT complex, is involved in the regulation of the spindle assembly checkpoint, suggesting that the CCR4-NOT complex also plays a part in the regulation of mitosis. CNOT3 depletion increases the population of mitotic-arrested cells and specifically increases the expression of MAD1 mRNA and its protein product that plays a part in the spindle assembly checkpoint. We showed that CNOT3 depletion stabilizes the MAD1 mRNA, and that MAD1 knockdown attenuates the CNOT3 depletion-induced increase of the mitotic index. Basing on these observations, we propose that CNOT3 is involved in the regulation of the spindle assembly checkpoint through its ability to regulate the stability of MAD1 mRNA.

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Citations

Dec 30, 2015·Cell Reports·Akinori TakahashiTadashi Yamamoto
Apr 3, 2016·Biochemical and Biophysical Research Communications·Ari ZukeranTadashi Yamamoto
Feb 26, 2016·Molecular Biology of the Cell·Maximilian BillmannMichael Boutros
Sep 6, 2014·Frontiers in Genetics·Yo-Taro ShiraiTadashi Yamamoto
Jun 16, 2017·Scientific Reports·Alfonso Rodríguez-GilM Lienhard Schmitz

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