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ZFIN ID: ZDB-PUB-031103-19
A cellular framework for gut-looping morphogenesis in zebrafish
Horne-Badovinac, S., Rebagliati, M., and Stainier, D.Y.
Date: 2003
Source: Science (New York, N.Y.)   302(5645): 662-665 (Journal)
Registered Authors: Horne-Badovinac, Sally, Rebagliati, Michael, Stainier, Didier
Keywords: none
MeSH Terms:
  • Animals
  • Body Patterning*
  • Cell Movement
  • Cues
  • Endoderm/physiology
  • Gene Expression Regulation, Developmental*
  • Guanylate Kinases
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/physiology
  • Intestines/embryology*
  • Isoenzymes
  • Mesoderm/cytology
  • Mesoderm/physiology
  • Morphogenesis
  • Mutation
  • Nuclear Proteins*
  • Nucleoside-Phosphate Kinase/genetics
  • Nucleoside-Phosphate Kinase/metabolism
  • Oligonucleotides, Antisense
  • Phenotype
  • Protein Kinase C/genetics
  • Protein Kinase C/physiology
  • Transcription Factors/genetics
  • Transcription Factors/physiology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology
PubMed: 14576439 Full text @ Science
Many vertebrate organs adopt asymmetric positions with respect to the midline, but little is known about the cellular changes and tissue movements that occur downstream of left-right gene expression to produce this asymmetry. Here, we provide evidence that the looping of the zebrafish gut results from the asymmetric migration of the neighboring lateral plate mesoderm (LPM). Mutations that disrupt the epithelial structure of the LPM perturb this asymmetric migration and inhibit gut looping. Asymmetric LPM migration still occurs when the endoderm is ablated from the gut-looping region, suggesting that the LPM can autonomously provide a motive force for gut displacement. Finally, reducing left-sided Nodal activity randomizes the pattern of LPM migration and gut looping. These results reveal a cellular framework for the regulation of organ laterality by asymmetrically expressed genes.