Manipulation of estrogen synthesis alters MIR202* expression in embryonic chicken gonads

Stephanie C. Bannister, Craig A. Smith, Kelly N Roeszler, Timothy J. Doran, Andrew H. Sinclair, Mark L V Tizard

Research output: Contribution to journalArticleResearchpeer-review

47 Citations (Scopus)

Abstract

Tissue-specific patterns of microRNA (miRNA) expression contribute to organogenesis during embryonic development. Using the embryonic chicken gonads as a model for vertebrate gonadogenesis, we previously reported that miRNAs are expressed in a sexually dimorphic manner during gonadal sex differentiation. Being male biased, we hypothesised that upregulation of microRNA 202* (MIR202*) is characteristic of testicular differentiation. To address this hypothesis, we used estrogen modulation to induce gonadal sex reversal in embryonic chicken gonads and analyzed changes in MIR202* expression. In ovo injection of estradiol-17beta at Embryonic Day 4.5 (E4.5) caused feminization of male gonads at E9.5 and reduced MIR202* expression to female levels. Female gonads treated at E3.5 with an aromatase inhibitor, which blocks estrogen synthesis, were masculinized by E9.5, and MIR202* expression was increased. Reduced MIR202* expression correlated with reduced expression of the testis-associated genes DMRT1 and SOX9, and up-regulation of ovary-associated genes FOXL2 and CYP19A1 (aromatase). Increased MIR202* expression correlated with down-regulation of FOXL2 and aromatase and up-regulation of DMRT1 and SOX9. These results confirm that up-regulation of MIR202* coincides with testicular differentiation in embryonic chicken gonads.

Original languageEnglish
Pages (from-to)22-30
Number of pages9
JournalBiology of Reproduction
Volume85
Issue number1
DOIs
Publication statusPublished - 1 Jul 2011
Externally publishedYes

Keywords

  • Aromatase inhibitor
  • Chicken embryo
  • E2
  • Estradiol-17β
  • Estradiol/estradiol receptor
  • Estrogen
  • Gonad
  • MicroRNA MIR202*
  • Sex determination
  • Testis

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