PUBLICATION

Laminin beta1a controls distinct steps during the establishment of digestive organ laterality

Authors
Hochgreb-Hägele, T., Yin, C., Koo, D.E., Bronner, M.E., and Stainier, D.Y.
ID
ZDB-PUB-130709-51
Date
2013
Source
Development (Cambridge, England)   140(13): 2734-2745 (Journal)
Registered Authors
Bronner-Fraser, Marianne, Stainier, Didier, Yin, Chunyue
Keywords
asymmetry, laminin, organogenesis
MeSH Terms
  • Animals
  • Body Patterning/genetics
  • Body Patterning/physiology
  • Cilia/metabolism
  • Functional Laterality/genetics
  • Functional Laterality/physiology
  • Gastrointestinal Tract/embryology
  • Gastrointestinal Tract/metabolism
  • Gene Expression Regulation, Developmental/genetics
  • Gene Expression Regulation, Developmental/physiology
  • Immunohistochemistry
  • In Situ Hybridization
  • Laminin/genetics
  • Laminin/metabolism*
  • Organogenesis/genetics
  • Organogenesis/physiology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
23757411 Full text @ Development
Abstract

Visceral organs, including the liver and pancreas, adopt asymmetric positions to ensure proper function. Yet the molecular and cellular mechanisms controlling organ laterality are not well understood. We identified a mutation affecting zebrafish laminin β1a (lamb1a) that disrupts left-right asymmetry of the liver and pancreas. In these mutants, the liver spans the midline and the ventral pancreatic bud remains split into bilateral structures. We show that lamb1a regulates asymmetric left-right gene expression in the lateral plate mesoderm (LPM). In particular, lamb1a functions in Kupffer’s vesicle (KV), a ciliated organ analogous to the mouse node, to control the length and function of the KV cilia. Later during gut-looping stages, dynamic expression of Lamb1a is required for the bilayered organization and asymmetric migration of the LPM. Loss of Lamb1a function also results in aberrant protrusion of LPM cells into the gut. Collectively, our results provide cellular and molecular mechanisms by which extracellular matrix proteins regulate left-right organ morphogenesis.

Genes / Markers
Figures
Figure Gallery
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Errata and Notes