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PABP cooperates with the CCR4-NOT complex to promote mRNA deadenylation and block precocious decay

Cited 62 time in Web of Science Cited 60 time in Scopus
Authors
Yi, Hyerim; Park, Joha; Ha, Minju; Lim, Jaechul; Chang, Hyeshik; Kim, V. Narry
Issue Date
2018-06
Citation
Molecular Cell, Vol.70 No.6, pp.1081-1088.e5
Abstract
Multiple deadenylases are known in vertebrates, the PAN2-PAN3 (PAN2/3) and CCR4-NOT (CNOT) complexes, and PARN, yet their differential functions remain ambiguous. Moreover, the role of poly(A) binding protein (PABP) is obscure, limiting our understanding of the deadenylation mechanism. Here, we show that CNOT serves as a predominant nonspecific deadenylase for cytoplasmic poly(A)+ RNAs, and PABP promotes deadenylation while preventing premature uridylation and decay. PAN2/3 selectively trims long tails (> similar to 150 nt) with minimal effect on transcriptome, whereas PARN does not affect mRNA deadenylation. CAF1 and CCR4, catalytic subunits of CNOT, display distinct activities: CAF1 trims naked poly(A) segments and is blocked by PABPC, whereas CCR4 is activated by PABPC to shorten PABPC-protected sequences. Concerted actions of CAF1 and CCR4 delineate the similar to 27 nt periodic PABPC footprints along shortening tail. Our study unveils distinct functions of deadenylases and PABPC, re-drawing the view on mRNA deadenylation and regulation.
ISSN
1097-2765
URI
https://hdl.handle.net/10371/171950
DOI
https://doi.org/10.1016/j.molcel.2018.05.009
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College of Natural Sciences (자연과학대학)Dept. of Biological Sciences (생명과학부)Journal Papers (저널논문_생명과학부)
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