Involvement of CNOT3 in mitotic progression through inhibition of MAD1 expression.

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.

authors

Takahashi A,Kikuguchi C,Morita M,Shimodaira T,Tokai-Nishizumi N,Yokoyama K,Ohsugi M,Suzuki T,Yamamoto T

doi

10.1016/j.bbrc.2012.02.007

subject

Has Abstract

pub_date

2012-03-09 00:00:00

pages

268-73

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)00225-2

journal_volume

419

pub_type

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