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7 September 2011 Minimal Fertility Defects in Mice Deficient in Oocyte-Expressed Smad4
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Abstract

Bidirectional signaling between oocytes and granulosa cells is required for normal folliculogenesis. Oocyte-secreted members of the transforming growth factor beta (TGFB) family, growth differentiation factor 9 (GDF9), and bone morphogenetic protein 15 (BMP15) are well-known mediators of granulosa cell function. Deletion in granulosa cells of Smad4, the common SMAD mediating all canonical TGFB-related protein signals, results in infertility. Reciprocal signaling by granulosa cell-expressed TGFB family ligands, such as activin, to the oocyte during follicle development has been proposed but not tested in vivo using conditional knockout mice. Therefore, we generated two oocyte-specific conditional knockout models for the common SMAD, Smad4, using cre recombinase expression from either the zona pellucida 3 (Zp3) or Gdf9 promoter. Cre expression from the Gdf9 promoter occurs at a slightly earlier time point in follicle development than from Zp3. Deletion of Smad4 using Zp3cre had no effect on fertility, while deletion of Smad4 with Gdf9icre resulted in a slight, but significant, reduction in litter size. These mouse models suggest a novel, although minor, role for Smad4 in the oocyte restricted to the primordial follicle stage.

Xiaohui Li, Swamy K. Tripurani, Rebecca James, and Stephanie A. Pangas "Minimal Fertility Defects in Mice Deficient in Oocyte-Expressed Smad4," Biology of Reproduction 86(1), (7 September 2011). https://doi.org/10.1095/biolreprod.111.094375
Received: 24 June 2011; Accepted: 1 August 2011; Published: 7 September 2011
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