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Reprod Toxicol. 2014 Jan;43:111-24. doi: 10.1016/j.reprotox.2013.12.002. Epub 2013 Dec 16.

Eye-specific gene expression following embryonic ethanol exposure in zebrafish: roles for heat shock factor 1.

Author information

1
Department of Biological Sciences, University of Idaho, Moscow, ID 83844, United States; Neuroscience Graduate Program, University of Idaho, Moscow, ID 83844, United States.
2
Department of Biological Sciences, University of Idaho, Moscow, ID 83844, United States.
3
School of Molecular Biosciences, Washington State University, Pullman, WA 99164, United States; Center for Reproductive Biology, University of Idaho, Moscow, ID 83844, United States.
4
Department of Biological Sciences, University of Idaho, Moscow, ID 83844, United States; Neuroscience Graduate Program, University of Idaho, Moscow, ID 83844, United States; Center for Reproductive Biology, University of Idaho, Moscow, ID 83844, United States. Electronic address: dstenkam@uidaho.edu.

Abstract

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.

KEYWORDS:

Ethanol; Eye; Fetal alcohol syndrome; Heat shock factor; Heat shock protein; Microarray; Retina; Zebrafish

PMID:
24355176
PMCID:
PMC3918430
DOI:
10.1016/j.reprotox.2013.12.002
[Indexed for MEDLINE]
Free PMC Article

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