ZFIN ID: ZDB-PUB-140220-10
Eye-specific gene expression following embryonic ethanol exposure in zebrafish: Roles for heat shock factor 1
Kashyap, B., Pegorsch, L., Frey, R.A., Sun, C., Shelden, E.A., and Stenkamp, D.L.
Date: 2014
Source: Reproductive toxicology (Elmsford, N.Y.) 43: 111-124 (Journal)
Registered Authors: Frey, Ruth, Shelden, Eric, Stenkamp, Deborah L.
Keywords: none
Microarrays: GEO:GSE51427
MeSH Terms:
  • Animals
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/metabolism
  • Ethanol/toxicity*
  • Eye/drug effects*
  • Eye/embryology
  • Eye/metabolism
  • Gene Expression Profiling
  • Gene Expression Regulation, Developmental/drug effects*
  • Microphthalmos/chemically induced*
  • Microphthalmos/genetics
  • Microphthalmos/metabolism
  • Oligonucleotide Array Sequence Analysis
  • Transcription Factors/genetics*
  • Transcription Factors/metabolism
  • Zebrafish/embryology
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed: 24355176 Full text @ Reprod. Toxicol.

The mechanisms through which ethanol exposure results in developmental defects remain unclear. We used the zebrafish model to elucidate eye-specific mechanisms that underlie ethanol-mediated microphthalmia (reduced eye size), through time-series microarray analysis of gene expression within eyes of embryos exposed to 1.5% ethanol. 62 genes were differentially expressed (DE) in ethanol-treated as compared to control eyes sampled during retinal neurogenesis (24–48 h post-fertilization). The EDGE (extraction of differential gene expression) algorithm identified >3000 genes DE over developmental time in ethanol-exposed eyes as compared to controls. The DE lists included several genes indicating a mis-regulated cellular stress response due to ethanol exposure. Combined treatment with sub-threshold levels of ethanol and a morpholino targeting heat shock factor 1 mRNA resulted in microphthalmia, suggesting convergent molecular pathways. Thermal preconditioning partially prevented ethanol-mediated microphthalmia while maintaining Hsf-1 expression. These data suggest roles for reduced Hsf-1 in mediating microphthalmic effects of embryonic ethanol exposure.