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Conditional deletion of Sox17 reveals complex effects on uterine adenogenesis and function
Journal article   Open access   Peer reviewed

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

Amy Guimarães-Young, Traci Neff, Adam J Dupuy and Michael J Goodheart
Developmental Biology, Vol.414(2), pp.219-227
06/15/2016
DOI: 10.1016/j.ydbio.2016.04.010
PMCID: PMC5521196
PMID: 27102016
url
https://doi.org/10.1016/j.ydbio.2016.04.010View
Published (Version of record) Open Access

Abstract

The importance of canonical Wnt signaling to murine uterine development is well established. Mouse models in which uterine-specific Wnt ligands, β-catenin, or Lef1 are disrupted result in failure of postnatal endometrial gland development. Sox17 is a transcription factor characterized in numerous tissues as an antagonist of Wnt signaling. Thus, we hypothesized that conditional ablation of Sox17 would lead to hyperproliferation of endometrial glands in mice. Contrary to our prediction, disruption of Sox17 in epithelial and stromal compartments led to inhibition of endometrial adenogenesis and a loss of reproductive capacity. Epithelium-specific Sox17 disruption resulted in normal adenogenesis although reproductive capacity remained impaired. These findings suggest that non-epithelial, Sox17-positive cells are necessary for adenogenesis and that glands require Sox17 to properly function. To our knowledge, these findings are the first to implicate Sox17 in endometrial gland formation and reproductive success. The data presented herein underscore the importance of studying Sox17 in uterine homeostasis and function. •Multi-compartment uterine Sox17 deletion impairs normal uterine function.•Non-epithelial, Sox17-positive stromal cells are necessary for gland formation.•Mice with Sox17-negative glandular cells are unable to reproduce.
Development Adenogenesis Mouse model Uterus Endometrial glands Sox17

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