PUBLICATION

Chd7 plays a critical role in controlling left-right symmetry during zebrafish somitogenesis

Authors
Jacobs-McDaniels, N.L., and Albertson, R.C.
ID
ZDB-PUB-110914-18
Date
2011
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   240(10): 2272-80 (Journal)
Registered Authors
Albertson, R. Craig
Keywords
somitogenesis, Chd7, zebrafish, development, laterality, spinal deformity
MeSH Terms
  • Animals
  • Body Patterning*
  • CHARGE Syndrome/genetics
  • DNA Helicases/genetics
  • DNA Helicases/metabolism*
  • DNA-Binding Proteins/genetics
  • DNA-Binding Proteins/metabolism*
  • Embryo, Nonmammalian/anatomy & histology*
  • Embryo, Nonmammalian/embryology*
  • Embryo, Nonmammalian/physiology
  • Humans
  • Oligonucleotides, Antisense/genetics
  • Oligonucleotides, Antisense/metabolism
  • Somites/anatomy & histology
  • Somites/embryology*
  • Somites/physiology
  • Spine/abnormalities
  • Zebrafish/anatomy & histology
  • Zebrafish/embryology*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
21901784 Full text @ Dev. Dyn.
Abstract

Somitogenesis is a complex process during early vertebrate development involving interactions between many factors to form a bilateral somite series. A role for chromatin remodelers in somitogenesis has not yet been demonstrated. Here, we investigate the function of chromodomain helicase DNA binding protein 7 (chd7) during zebrafish somitogenesis. We show that Chd7 deficiency leads to asymmetric segmentation of the presomitic mesoderm (PSM), as revealed by expression of the somitogenesis genes, cdx1a, dlc, her7, mespa, and ripply1. Moreover, we show that abrogation of Chd7 results in the loss of asymmetric expression of spaw in the lateral plate mesoderm, which is consistent with more general laterality defects. Based on the observation that insufficient Chd7 leads to left–right asymmetry defects during PSM segmentation, and because CHD7 has been linked to human spinal deformities, we suggest that zebrafish chd7 morphants may be a good in vivo model to examine the pathophysiology of these diseases.

Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping