ZFIN ID: ZDB-PUB-090204-7
FGF-dependent left-right asymmetry patterning in zebrafish is mediated by Ier2 and Fibp1
Hong, S.K., and Dawid, I.B.
Date: 2009
Source: Proceedings of the National Academy of Sciences of the United States of America   106(7): 2230-2235 (Journal)
Registered Authors: Dawid, Igor B., Hong, Sung-Kook
Keywords: ciliogenesis, Kupffer's vesicle, laterality
MeSH Terms:
  • Animals
  • Body Patterning*
  • Carrier Proteins/genetics
  • Carrier Proteins/physiology*
  • Cell Line
  • Developmental Biology
  • Fibroblast Growth Factors/metabolism*
  • Gene Expression Regulation, Developmental*
  • Humans
  • Immediate-Early Proteins/genetics
  • Immediate-Early Proteins/physiology*
  • In Situ Hybridization
  • Models, Biological
  • Phenotype
  • RNA, Messenger/metabolism
  • Two-Hybrid System Techniques
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Zebrafish Proteins/physiology
PubMed: 19164561 Full text @ Proc. Natl. Acad. Sci. USA
Establishment of left-right asymmetry in vertebrates requires nodal, Wnt-PCP and FGF signaling and involves ciliogenesis in a laterality organ. Effector genes through which FGF signaling affects laterality have not been described. We isolated the zebrafish ier2 and fibp1 genes as FGF target genes and show that their protein products interact. Knock down of these factors interferes with establishment of organ laterality and causes defective cilia formation in Kupffer's Vesicle, the zebrafish laterality organ. Cilia are also lost after suppression of FGF8, but can be rescued by injection of ier2 and fibp1 mRNA. We conclude that Ier2 and Fibp1 mediate FGF signaling in ciliogenesis in Kupffer's Vesicle and in the establishment of laterality in the zebrafish embryo.