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Alterations in the developing testis transcriptome following embryonic vinclozolin exposure.

Tracy M Clement1, Marina I Savenkova, Matthew Settles

  • 1Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-4236, USA.

Reproductive Toxicology (Elmsford, N.Y.)
|June 23, 2010
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Prenatal exposure to vinclozolin alters gene expression in developing rat testes. These transient changes in the F1 generation suggest epigenetic mechanisms and signaling pathways are involved in vinclozolin

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Area of Science:

  • Reproductive Toxicology
  • Developmental Biology
  • Epigenetics

Background:

  • Vinclozolin exposure during embryonic development causes epigenetic modifications.
  • These modifications lead to transgenerational adult-onset disease states.
  • The direct effects on the F1 generation's developing testes require further investigation.

Purpose of the Study:

  • To investigate the direct effects of in utero vinclozolin exposure on the F1 generation rat testis transcriptome.
  • To identify differentially expressed genes and associated pathways in response to vinclozolin.
  • To explore the role of epigenetic mechanisms and signaling pathways in vinclozolin's developmental toxicity.

Main Methods:

  • Microarray analysis of rat testis transcriptomes.
  • Comparison of control and vinclozolin-treated groups at embryonic days 13, 14, and 16.
  • Analysis of differentially expressed genes and associated cellular functions and pathways.

Main Results:

  • Identified 576 differentially expressed genes in the F1 generation rat testes.
  • Observed transient and distinct sets of regulated genes at different developmental stages.
  • Gene expression alterations suggest involvement of Wnt and calcium signaling, vascular development, and epigenetic mechanisms.

Conclusions:

  • In utero vinclozolin exposure directly impacts the F1 generation rat testis transcriptome.
  • The observed gene expression changes are transient and stage-specific.
  • Wnt/calcium signaling, vascular development, and epigenetic modifications are potential mediators of vinclozolin's effects.