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Multiple tissue-specific epigenetic alterations regulate persistent gene expression changes following developmental

Tanner B Jefferson1, Tianyuan Wang2, Wendy N Jefferson1

  • 1Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, 27709, USA.

Epigenetics
|November 3, 2022
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Summary

Developmental exposure to diethylstilboestrol (DES) alters reproductive tract development. This study reveals DES reprograms gene expression via epigenetic changes like histone modification and DNA methylation, impacting seminal vesicles and distinct from uterine tissue effects.

Keywords:
Estrogen receptorhistone modificationmouse seminal vesiclesneonatal DES exposuretranscriptome

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Area of Science:

  • Reproductive Biology
  • Endocrinology
  • Epigenetics

Background:

  • Developmental exposure to endocrine disruptors like diethylstilboestrol (DES) causes reproductive abnormalities.
  • Neonatal DES exposure alters seminal vesicle (SV) transcriptome and DNA methylation via estrogen receptor alpha (ERα).
  • The role of histone modifications in DES-induced SV transcriptome alterations remains unclear.

Purpose of the Study:

  • To investigate the contribution of histone modifications to DES-induced transcriptome changes in developing mouse seminal vesicles.
  • To analyze genome-wide DNA methylation and H3K27ac patterns in response to developmental DES exposure.
  • To compare epigenetic reprogramming in SVs and uterine tissue following neonatal DES exposure.

Main Methods:

  • Genome-wide analysis of mRNA, lncRNA, DNA methylation, and H3K27ac in mouse SVs.
  • Experiments utilized wild-type and ERα knockout mice exposed to DES during development.
  • Comparative analysis of epigenetic marks and gene expression in SV and uterine tissues.

Main Results:

  • Neonatal DES exposure altered ERα-mediated gene expression in adult SVs, including genes involved in chromatin modification.
  • Both DNA methylation and H3K27ac patterns were reprogrammed during SV development and after DES exposure, with some ERα-dependent and independent changes.
  • DES-induced epigenetic changes and gene alterations were largely distinct between SV and uterine tissues.

Conclusions:

  • Developmental DES exposure reprograms reproductive tract differentiation through multiple epigenetic mechanisms.
  • Histone modifications, particularly H3K27ac at enhancers, contribute to DES-induced transcriptome alterations in SVs.
  • Epigenetic effects of developmental DES exposure are tissue-specific, impacting SVs differently than uterine tissue.