ZFIN ID: ZDB-PUB-130416-12
Bmp and Shh Signaling Mediate the Expression of satb2 in the Pharyngeal Arches
Sheehan-Rooney, K., Swartz, M.E., Lovely, C.B., Dixon, M.J., and Eberhart, J.K.
Date: 2013
Source: PLoS One   8(3): e59533 (Journal)
Registered Authors: Dixon, Monica, Eberhart, Johann, Sheehan-Rooney, Kelly, Swartz, Mary
Keywords: none
MeSH Terms:
  • Animals
  • Bone Morphogenetic Proteins/metabolism*
  • Branchial Region/cytology*
  • Branchial Region/embryology
  • Branchial Region/metabolism*
  • Endoderm/cytology
  • Endoderm/metabolism
  • Gene Expression Regulation, Developmental*
  • Hedgehog Proteins/metabolism*
  • Matrix Attachment Region Binding Proteins/metabolism*
  • Neural Crest/cytology
  • Neural Crest/metabolism
  • Signal Transduction*
  • Transcription Factors/metabolism*
  • Zebrafish/embryology
  • Zebrafish Proteins/metabolism*
PubMed: 23555697 Full text @ PLoS One

In human, mutation of the transcription factor SATB2 causes severe defects to the palate and jaw. The expression and sequence of SATB2 is highly conserved across vertebrate species, including zebrafish. We sought to understand the regulation of satb2 using the zebrafish model system. Due to the normal expression domains of satb2, we analyzed satb2 expression in mutants with disrupted Hh signaling or defective ventral patterning. While satb2 expression appears independent of Edn1 signaling, appropriate expression requires Shha, Smo, Smad5 and Hand2 function. Transplantation experiments show that neural crest cells receive both Bmp and Hh signaling to induce satb2 expression. Dorsomorphin- and cyclopamine-mediated inhibition of Bmp and Hh signaling, respectively, suggests that proper satb2 expression requires a relatively earlier Bmp signal and a later Hh signal. We propose that Bmp signaling establishes competence for the neural crest to respond to Hh signaling, thus inducing satb2 expression.