ZFIN ID: ZDB-PUB-120529-27
MicroRNA-206 regulates cell movements during zebrafish gastrulation by targeting prickle1a and regulating JNK2 phosphorylation
Liu, X., Ning, G., Meng, A., and Wang, Q.
Date: 2012
Source: Molecular and cellular biology   32(14): 2934-2942 (Journal)
Registered Authors: Meng, Anming
Keywords: none
MeSH Terms:
  • Actin Cytoskeleton/metabolism
  • Adaptor Proteins, Signal Transducing/genetics*
  • Adaptor Proteins, Signal Transducing/metabolism
  • Animals
  • Animals, Genetically Modified
  • Base Sequence
  • Cell Movement/genetics
  • Cell Movement/physiology
  • Cell Surface Extensions/metabolism
  • Gastrulation/genetics
  • Gastrulation/physiology
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • LIM Domain Proteins/genetics*
  • LIM Domain Proteins/metabolism
  • MicroRNAs/antagonists & inhibitors
  • MicroRNAs/genetics*
  • MicroRNAs/metabolism
  • Mitogen-Activated Protein Kinase 9/metabolism*
  • Phosphorylation
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Signal Transduction
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed: 22615492 Full text @ Mol. Cell. Biol.

During vertebrate gastrulation, both concurrent inductive events and cell movements are required for axis formation. Convergence and extension (CE) movements contribute to narrowing and lengthening the forming embryonic axis. MicroRNAs (miRNAs) play a critical role in regulating fundamental cellular functions and developmental processes, but their functions in CE movements are not well known. Zebrafish mir206 is maternally expressed and are present throughout blastulation and gastrulation periods. Either gain- or loss-of-function of mir206 leads to severe defects of convergent extension movements both cell-autonomously and non-cell-autonomously. Mosaic lineage tracing studies reveal that the formation of membrane protrusions and actin filaments is disturbed in mir206-overexpressing embryos or mir206 morphants. Mechanistically, mir206 targets prickle1a (pk1a) mRNA and as a result regulates JNK2 phosphorylation. pk1a overexpression or knockdown can rescue convergent extension defects induced by mir206 overexpression or knockdown, respectively. Therefore, mir206 is an essential, novel regulator for normal convergent and extension movements by regulating MAPK JNK signaling.