PUBLICATION

m6A-dependent maternal mRNA clearance facilitates zebrafish maternal-to-zygotic transition.

Authors
Zhao, B.S., Wang, X., Beadell, A.V., Lu, Z., Shi, H., Kuuspalu, A., Ho, R.K., He, C.
ID
ZDB-PUB-170214-2
Date
2017
Source
Nature   542(7642): 475-478 (Journal)
Registered Authors
Beadell, Alana, He, Chuan, Ho, Robert K., Wang, Xiao, Zhao, Boxuan
Keywords
RNA, Epigenetics, Embryogenesis
Datasets
GEO:GSE79213
MeSH Terms
  • Adenosine/analogs & derivatives*
  • Adenosine/metabolism
  • Animals
  • Embryonic Development/genetics*
  • Female
  • Male
  • RNA Stability*
  • RNA, Messenger, Stored/chemistry
  • RNA, Messenger, Stored/genetics
  • RNA, Messenger, Stored/metabolism*
  • RNA-Binding Proteins/genetics
  • RNA-Binding Proteins/metabolism
  • Time Factors
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Zygote/metabolism*
PubMed
28192787 Full text @ Nature
Abstract
The maternal-to-zygotic transition (MZT) is one of the most profound and tightly orchestrated processes during the early life of embryos, yet factors that shape the temporal pattern of vertebrate MZT are largely unknown. Here we show that over one-third of zebrafish maternal messenger RNAs (mRNAs) can be N6-methyladenosine (m6A) modified, and the clearance of these maternal mRNAs is facilitated by an m6A-binding protein, Ythdf2. Removal of Ythdf2 in zebrafish embryos decelerates the decay of m6A-modified maternal mRNAs and impedes zygotic genome activation. These embryos fail to initiate timely MZT, undergo cell-cycle pause, and remain developmentally delayed throughout larval life. Our study reveals m6A-dependent RNA decay as a previously unidentified maternally driven mechanism that regulates maternal mRNA clearance during zebrafish MZT, highlighting the critical role of m6A mRNA methylation in transcriptome switching and animal development.
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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Mapping