Published by Oxford University Press 2006.
Casting a Broad Network: Fishing for Mechanisms of Retinoid Teratogenicity
Developmental Biology Branch, Reproductive Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711
1For correspondence via e-mail: rogers.john@epa.gov.
Received September 6, 2006; accepted September 7, 2006
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In this issue, Ali-Khan et al. (pages 139–152) have used gene expression analysis to elucidate signaling pathways potentially involved in the mechanism of the developmental toxicity of excess vitamin A (retinol acetate). The ability to examine simultaneously the expression of thousands of genes in a tissue of interest has emerged relatively recently. While some have characterized the use of this technology to elucidate mechanisms of toxicity as "fishing trips," the approach can be powerful for generating hypotheses. Global gene array analysis has been used to some success in identifying developmental pathways affected by the human and murine teratogen, valproic acid (Kultima et al., 2004
; Okada and Fujiwara, 2006), and has also been used for expression profiling across normal developmental stages