Conditional deletion of Sox17 reveals complex effects on uterine adenogenesis and function

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Amy Guimarães-Young1, Traci Neff2, Adam J Dupuy1

  • 1Department of Anatomy and Cell Biology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.

Developmental Biology
|April 23, 2016
PubMed

Insights

Sox17 normally promotes mouse uterine gland development and reproductive success. Unexpectedly, removing Sox17 inhibited gland formation and fertility, highlighting its crucial role in uterine homeostasis.

Area of Science:

  • Reproductive Biology
  • Developmental Biology
  • Endocrinology

Background:

  • Canonical Wnt signaling is vital for murine uterine development, with disruptions in Wnt ligands, β-catenin, or Lef1 impairing endometrial gland formation.
  • Sox17 is known to antagonize Wnt signaling in various tissues.

Purpose of the Study:

  • To investigate the role of Sox17 in uterine development and function by examining the effects of its conditional ablation.
  • To test the hypothesis that Sox17 ablation would lead to hyperproliferation of endometrial glands.

Main Methods:

  • Conditional ablation of Sox17 in mouse uterine epithelial and stromal compartments.
  • Assessment of endometrial adenogenesis (gland development).
  • Evaluation of reproductive capacity in genetically modified mice.

Main Results:

  • Contrary to the hypothesis, Sox17 disruption inhibited endometrial adenogenesis and caused a loss of reproductive capacity.
  • Epithelium-specific Sox17 disruption led to normal adenogenesis but impaired reproductive capacity.
  • These results indicate a non-epithelial role for Sox17 in adenogenesis and gland function.

Conclusions:

  • Sox17 is essential for normal endometrial gland development and reproductive success in mice.
  • Non-epithelial Sox17-positive cells are critical for adenogenesis.
  • Sox17 plays a previously unrecognized role in uterine homeostasis and function.
Keywords:
AdenogenesisDevelopmentEndometrial glandsMouse modelSox17Uterus

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