ZFIN ID: ZDB-PUB-141206-7
Comparative analysis of genes regulated by Dzip1/iguana and Hedgehog in zebrafish
Arnold, C.R., Lamont, R.E., Walker, J.T., Spice, P.J., Chan, C.K., Ho, C.Y., Childs, S.J.
Date: 2015
Source: Developmental dynamics : an official publication of the American Association of Anatomists 244(2): 211-23 (Journal)
Registered Authors: Childs, Sarah J., Ho, Chi-Yip, Lamont, Ryan
Keywords: Microarray, cyclopamine, hemorrhage
MeSH Terms:
  • Animals
  • Carrier Proteins/genetics
  • Carrier Proteins/metabolism*
  • Gene Expression Regulation, Developmental/physiology*
  • Hedgehog Proteins/genetics
  • Hedgehog Proteins/metabolism*
  • Neovascularization, Physiologic/physiology*
  • Signal Transduction/physiology*
  • Transcriptional Activation/physiology
  • Zebrafish/embryology*
  • Zebrafish/genetics
PubMed: 25476803 Full text @ Dev. Dyn.
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ABSTRACT
Background: The zebrafish genetic mutant iguana (igu) has defects in the ciliary basal body protein Dzip1, causing improper cilia formation. Dzip1 also interacts with the downstream transcriptional activators of Hedgehog (Hh), the Gli proteins, and Hh signaling is disrupted in igu mutants. Hh governs a wide range of developmental processes, including stabilizing developing blood vessels to prevent hemorrhage. Using igu mutant embryos and embryos treated with the Hh pathway antagonist cyclopamine, we conducted a microarray to determine genes involved in Hh signalling mediating vascular stability. Results: We identified 40 genes with significantly altered expression in both igu mutants and cyclopamine-treated embryos. For a subset of these, we used in situ hybridization to determine localization during embryonic development and confirm the expression changes seen on the array. Conclusions: Through comparing gene expression changes in a genetic model of vascular instability with a chemical inhibition of Hh signalling, we identified a set of 40 differentially expressed genes with potential roles in vascular stabilization. This article is protected by copyright. All rights reserved.
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