PUBLICATION

Retinoic acid-mediated gene expression in transgenic reporter zebrafish

Authors
Perz-Edwards, A., Hardison, N.L., and Linney, E.
ID
ZDB-PUB-010130-1
Date
2001
Source
Developmental Biology   229(1): 89-101 (Journal)
Registered Authors
Hardison, Nancy, Linney, Elwood, Perz-Edwards, Alyssa
Keywords
retinoic acid; RARE; zebrafish; transgenic; neural tube; retina; heart; diethylaminobenzaldehyde
MeSH Terms
  • Aldehyde Oxidoreductases/genetics
  • Animals
  • Benzaldehydes/toxicity
  • Cell Communication
  • Cytochrome P-450 Enzyme Inhibitors
  • Gastrula/drug effects
  • Gene Expression Regulation, Developmental*
  • Genes, Reporter*
  • Genetic Engineering
  • Monoterpenes*
  • Oxygenases/antagonists & inhibitors
  • Promoter Regions, Genetic
  • Retinal Dehydrogenase
  • Teratogens/toxicity
  • Terpenes/toxicity
  • Transcriptional Activation
  • Transgenes
  • Tretinoin/metabolism*
  • Vitamin A Deficiency
  • Zebrafish/genetics*
  • Zebrafish Proteins
PubMed
11133156 Full text @ Dev. Biol.
Abstract
Retinoic acid-mediated gene activation is important for normal vertebrate development. The size and nature of retinoic acid make it difficult to identify the precise cellular location of this signaling molecule throughout an embryo. Additionally, retinoic acid (RA) signaling is regulated by a complex combination of receptors, coactivators, and antagonizing proteins. Thus, in order to integrate these signals and identify regions within a whole developing embryo where cells can respond transcriptionally to retinoic acid, we have useda reporter transgenic approach. We have generated several stable lines of transgenic zebrafish which use retinoic acid response elements to drive fluorescent protein expression. In these zebrafish lines, transgene expression is localized to regions of the neural tube, retina, notochord, somites, heart, pronephric ducts, branchial arches, and jaw muscles in embryos and larvae. Transgene expression can be induced in additional regions of the neural tube and retina as well as the immature notochord, hatching gland, enveloping cell layer, and fin by exposing embryos to retinoic acid. Treatment with retinoic acid synthase inhibitors, citral and diethylaminobenzaldehyde (DEAB), during neurulation, greatly reduces transgene expression. DEAB treatment of embryos at gastrulation phenocopies the embryonic effects of vitamin A deprivation or targeted disruption of the RA synthase retinaldehyde dehydrogenase-2 in other vertebrates. Together these data suggest that the reporter expression we see in zebrafish is dependent upon conserved vertebrate pathways of RA synthesis.
Genes / Markers
Figures
Figure Gallery
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Errata and Notes