PUBLICATION

The T box transcription factor no tail in ciliated cells controls zebrafish left-right asymmetry

Authors
Amack, J.D., and Yost, H.J.
ID
ZDB-PUB-040416-4
Date
2004
Source
Current biology : CB   14(8): 685-690 (Journal)
Registered Authors
Amack, Jeffrey, Yost, H. Joseph
Keywords
none
MeSH Terms
  • Animals
  • Body Patterning/genetics
  • Body Patterning/physiology*
  • Cilia/physiology
  • Embryo, Nonmammalian/physiology
  • Epithelial Cells/physiology
  • Fetal Proteins
  • Gene Expression*
  • Gene Silencing
  • Immunohistochemistry
  • In Situ Hybridization
  • Microscopy, Fluorescence
  • Oligonucleotides
  • T-Box Domain Proteins/genetics
  • T-Box Domain Proteins/physiology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed
15084283 Full text @ Curr. Biol.
Abstract
The heart, brain, and gut develop essential left-right (LR) asymmetries. Specialized groups of ciliated cells have been implicated in LR patterning in mouse, chick, frog, and zebrafish embryos. In zebrafish, these ciliated cells are found in Kupffer's vesicle (KV) and are progeny of dorsal forerunner cells (DFCs). However, there is no direct evidence in any vertebrate that the genes involved in LR development are specifically required in ciliated cells. By using a novel method in zebrafish, we knocked down the function of no tail (ntl, homologous to mouse brachyury) in DFCs without affecting its expression in other cells in the embryo. We find that the Ntl transcription factor functions cell autonomously in DFCs to regulate KV morphogenesis and LR determination. This is the first evidence that loss-of-gene function exclusively in ciliated cells perturbs vertebrate LR patterning. Our results demonstrate that the ciliated KV, a transient embryonic organ of previously unknown function, is involved in the earliest known step in zebrafish LR development, suggesting that a ciliary-based mechanism establishes the LR axis in all vertebrate embryos.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping