TY - JOUR
T1 - Involvement of CNOT3 in mitotic progression through inhibition of MAD1 expression
AU - Takahashi, Akinori
AU - Kikuguchi, Chisato
AU - Morita, Masahiro
AU - Shimodaira, Tetsuhiro
AU - Tokai-Nishizumi, Noriko
AU - Yokoyama, Kazumasa
AU - Ohsugi, Miho
AU - Suzuki, Toru
AU - Yamamoto, Tadashi
N1 - Funding Information:
A.T. and T.Y. designed this study and wrote the manuscript. A.T. and C.K. performed the experiments, and A.T. analyzed the data. A.T. and T.Y. communicated with M.M., T.S., N.T., K.Y., M.O., and T.S. about data interpretation and writing of the manuscript. This work was supported by a grant-in-aid from the Japan Society for the Promotion of Science (JSPS) and the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) , Japan, by a research fellowship from JSPS for Young Scientists, and by the Global COE Program (Integrative Life Science Based on the Study of Biosignaling Mechanisms), MEXT, Japan.
PY - 2012/3/9
Y1 - 2012/3/9
N2 - 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.
AB - 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.
KW - CCR4-NOT complex
KW - CNOT3
KW - MAD1
KW - Mitosis
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U2 - 10.1016/j.bbrc.2012.02.007
DO - 10.1016/j.bbrc.2012.02.007
M3 - Article
C2 - 22342980
AN - SCOPUS:84862813787
SN - 0006-291X
VL - 419
SP - 268
EP - 273
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -