PUBLICATION

Ribosome Profiling Shows That miR-430 Reduces Translation Before Causing mRNA Decay in Zebrafish

Authors
Bazzini, A.A., Lee, M.T., and Giraldez, A.J.
ID
ZDB-PUB-120326-4
Date
2012
Source
Science (New York, N.Y.)   336(6078): 233-237 (Journal)
Registered Authors
Giraldez, Antonio, Lee, Miler
Keywords
none
Datasets
GEO:GSE34743
MeSH Terms
  • 3' Untranslated Regions
  • Animals
  • Embryo, Nonmammalian/metabolism
  • Embryonic Development
  • Gene Expression Regulation, Developmental
  • MicroRNAs/genetics*
  • MicroRNAs/metabolism
  • Peptide Chain Initiation, Translational*
  • Poly A/metabolism
  • Protein Biosynthesis
  • RNA Stability*
  • RNA, Messenger/metabolism*
  • Ribonuclease III/genetics
  • Ribosomes/metabolism*
  • Zebrafish/embryology
  • Zebrafish/genetics*
  • Zebrafish/metabolism
  • Zebrafish Proteins/biosynthesis
  • Zebrafish Proteins/genetics
PubMed
22422859 Full text @ Science
Abstract

MicroRNAs (miRNAs) regulate gene expression through deadenylation, repression, and messenger RNA (mRNA) decay. However, the contribution of each mechanism in non-steady-state situations remains unclear. We monitored the impact of miR-430 on ribosome occupancy of endogenous mRNAs in wild-type and dicer mutant zebrafish embryos. We find that miR-430 reduces the number of ribosomes on target mRNAs before causing mRNA decay. Translational repression occurs before complete deadenylation, and disrupting deadenylation using an internal poly(A) tail did not block target repression. Finally, we observe that ribosome density along the length of the message remains constant, suggesting that translational repression occurs by reducing the rate of initiation rather than affecting elongation or causing ribosomal drop-off. These results show that miR-430 regulates translation initiation before inducing mRNA decay during zebrafish development.

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Human Disease / Model
Sequence Targeting Reagents
Fish
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Mapping