PABP Cooperates with the CCR4-NOT Complex to Promote mRNA Deadenylation and Block Precocious Decay

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dc.contributor.authorHyerim Yi-
dc.contributor.authorJoha Park-
dc.contributor.authorMinju Ha-
dc.contributor.authorJaechul Lim-
dc.contributor.authorHyeshik Chang-
dc.contributor.authorV. Narry Kim-
dc.date.available2018-07-18T02:02:25Z-
dc.date.created2018-06-22-
dc.date.issued2018-06-
dc.identifier.issn1097-2765-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/4494-
dc.description.abstractMultiple 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 (>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 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. (c) 2018 Elsevier Inc-
dc.languageENG-
dc.publisherCELL PRESS-
dc.titlePABP Cooperates with the CCR4-NOT Complex to Promote mRNA Deadenylation and Block Precocious Decay-
dc.typeArticle-
dc.type.rimsA-
dc.identifier.wosid000436640300012-
dc.identifier.scopusid2-s2.0-85048205542-
dc.contributor.affiliatedAuthorHyerim Yi-
dc.contributor.affiliatedAuthorV. Narry Kim-
dc.identifier.bibliographicCitationMOLECULAR CELL, v.70, no.6, pp.1081 - 1088-
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Center for RNA Research(RNA 연구단) > Journal Papers (저널논문)
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