PUBLICATION

Unilateral dampening of bmp activity by nodal generates cardiac left-right asymmetry

Authors
Veerkamp, J., Rudolph, F., Cseresnyes, Z., Priller, F., Otten, C., Renz, M., Schaefer, L., and Abdelilah-Seyfried, S.
ID
ZDB-PUB-130405-5
Date
2013
Source
Developmental Cell   24(6): 660-667 (Journal)
Registered Authors
Abdelilah-Seyfried, Salim
Keywords
none
Datasets
GEO:GSE43888
MeSH Terms
  • Animals
  • Body Patterning/genetics*
  • Bone Morphogenetic Proteins/genetics
  • Bone Morphogenetic Proteins/metabolism*
  • Cell Movement
  • Gene Expression Regulation, Developmental
  • Glucuronosyltransferase/metabolism
  • Heart/embryology*
  • Left-Right Determination Factors*
  • Nodal Protein/metabolism*
  • Nonmuscle Myosin Type IIA
  • Nonmuscle Myosin Type IIB
  • Signal Transduction
  • Zebrafish
  • Zebrafish Proteins/metabolism
PubMed
23499359 Full text @ Dev. Cell
Abstract

Signaling by Nodal and Bmp is essential for cardiac laterality. How activities of these pathways translate into left-right asymmetric organ morphogenesis is largely unknown. We show that, in zebrafish, Nodal locally reduces Bmp activity on the left side of the cardiac field. This effect is mediated by the extracellular matrix enzyme Hyaluronan synthase 2, expression of which is induced by Nodal. Unilateral reduction of Bmp signaling results in lower expression of nonmuscle myosin II and higher cell motility on the left, driving asymmetric displacement of the entire cardiac field. In silico modeling shows that left-right differences in cell motility are sufficient to induce a robust, directional migration of cardiac tissue. Thus, the mechanism underlying the formation of cardiac left-right asymmetry involves Nodal modulating an antimotogenic Bmp activity.

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