2015 journal article

Gene-Specific Translation Regulation Mediated by the Hormone-Signaling Molecule EIN2

CELL, 163(3), 684–697.

By: C. Merchante  n, J. Brumos  n, J. Yun n, Q. Hu n, K. Spencer n, P. Enriquez n, B. Binder *, S. Heber n , A. Stepanova n , J. Alonso  n

MeSH headings : 3' Untranslated Regions; Arabidopsis / genetics; Arabidopsis / metabolism; Arabidopsis Proteins / genetics; Arabidopsis Proteins / metabolism; DNA-Binding Proteins; Ethylenes / metabolism; F-Box Proteins / genetics; Gene Expression Regulation, Plant; Nuclear Proteins / metabolism; Protein Biosynthesis; RNA, Messenger / metabolism; Receptors, Cell Surface / metabolism; Ribosomes / metabolism; Signal Transduction; Transcription Factors / metabolism
TL;DR: Characterization of one of the targets of this translation regulatory machinery, the ethylene signaling component EBF2, indicates that the signaling molecule EIN2 and the nonsense-mediated decay proteins UPFs play a central role in this ethylene-induced translational response. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

The central role of translation in modulating gene activity has long been recognized, yet the systematic exploration of quantitative changes in translation at a genome-wide scale in response to a specific stimulus has only recently become technically feasible. Using the well-characterized signaling pathway of the phytohormone ethylene and plant-optimized genome-wide ribosome footprinting, we have uncovered a molecular mechanism linking this hormone's perception to the activation of a gene-specific translational control mechanism. Characterization of one of the targets of this translation regulatory machinery, the ethylene signaling component EBF2, indicates that the signaling molecule EIN2 and the nonsense-mediated decay proteins UPFs play a central role in this ethylene-induced translational response. Furthermore, the 3'UTR of EBF2 is sufficient to confer translational regulation and required for the proper activation of ethylene responses. These findings represent a mechanistic paradigm of gene-specific regulation of translation in response to a key growth regulator.