PUBLICATION

Shh signalling restricts the expression of Gcm2 and controls the position of the developing parathyroids

Authors
Grevellec, A., Graham, A., and Tucker, A.S.
ID
ZDB-PUB-110316-33
Date
2011
Source
Developmental Biology   353(2): 194-205 (Journal)
Registered Authors
Keywords
Parathyroid, Gcm2, Shh, Pharyngeal pouch
MeSH Terms
  • Animals
  • Avian Proteins/deficiency
  • Avian Proteins/genetics
  • Avian Proteins/metabolism
  • Branchial Region/embryology
  • Branchial Region/metabolism
  • Chick Embryo
  • DNA-Binding Proteins/genetics
  • DNA-Binding Proteins/metabolism
  • Female
  • Gene Expression Regulation, Developmental/drug effects
  • Hedgehog Proteins/deficiency
  • Hedgehog Proteins/genetics
  • Hedgehog Proteins/metabolism*
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism
  • In Situ Hybridization, Fluorescence
  • Mice
  • Mice, Knockout
  • Mutation
  • Nuclear Proteins/genetics
  • Nuclear Proteins/metabolism
  • Parathyroid Glands/abnormalities
  • Parathyroid Glands/embryology*
  • Parathyroid Glands/metabolism*
  • Parathyroid Hormone/genetics
  • Parathyroid Hormone/metabolism
  • Pregnancy
  • Receptors, Calcium-Sensing/genetics
  • Receptors, Calcium-Sensing/metabolism
  • Receptors, Cell Surface/genetics
  • Receptors, Cell Surface/metabolism
  • Signal Transduction
  • Species Specificity
  • Transcription Factors/genetics
  • Transcription Factors/metabolism*
  • Veratrum Alkaloids/pharmacology
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
21349263 Full text @ Dev. Biol.
Abstract
The parathyroid glands originate from the endoderm of the caudal pharyngeal pouches. How these parathyroids are restricted to developing in the caudal pouches is unclear. In this paper we investigate the role of Shh signalling in patterning the vertebrate pharyngeal pouches, and show that Hh signalling may be involved in restricting the expression of the parathyroid marker Gcm2 in the pharyngeal epithelium. In the chick and mouse, Shh signalling is excluded or highly reduced in the posterior/caudal pouches, where the parathyroid marker Gcm2 is expressed, while remaining at high levels in the more anterior pouches. Moreover, though the block of Shh signalling at early developmental stages results in the loss of chick Gcm2 expression, at later stages, it induces ectopic Gcm2 expression domains in the second and first pharyngeal epithelium, suggesting that HH signalling prevents Gcm2 in those tissues. These ectopic domains go on to express other parathyroid markers but do not migrate and develop into ectopic parathyroids. Differences in the expression of Gcm2 in the chick, mouse and zebrafish, correlate with changing patterns of Shh signalling, indicating a conserved regulatory mechanism that acts to define pouch derivatives.
Genes / Markers
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping