| First Author | Li X | Year | 2012 |
| Journal | Biol Reprod | Volume | 86 |
| Issue | 1 | Pages | 1-6 |
| PubMed ID | 21900682 | Mgi Jnum | J:185785 |
| Mgi Id | MGI:5429848 | Doi | 10.1095/biolreprod.111.094375 |
| Citation | Li X, et al. (2012) Minimal fertility defects in mice deficient in oocyte-expressed Smad4. Biol Reprod 86(1):1-6 |
| abstractText | 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. |
