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Transforming growth factor β (TGFβ) signaling plays critical roles in reproductive development and function. TGFβ ligands signal through the TGFβ receptor type 2 (TGFBR2)/TGFBR1 complex. As TGFBR2 and TGFBR1 form a signaling complex upon ligand stimulation, they are expected to be equally important for propagating TGFβ signaling that elicits cellular responses. However, several genetic studies challenge this concept and indicate that disruption of TGFBR2 or TGFBR1 may lead to contrasting phenotypic outcomes. We have shown that conditional deletion of  Tgfbr1  using anti-Mullerian hormone receptor type 2 ( Amhr2 )-Cre causes oviductal and myometrial defects. To determine the functional requirement of TGFBR2 in the female reproductive tract and the potential phenotypic divergence/similarity resulting from conditional ablation of either receptor, we generated mice harboring  Tgfbr2  deletion using the same Cre driver that was previously employed to target  Tgfbr1 . Herein, we found that conditional deletion of  Tgfbr2  led to a similar phenotype to that of  Tgfbr1  deletion in the female reproductive tract. Furthermore, genetic removal of  Tgfbr1  in the  Tgfbr2 -deleted uterus had minimal impact on the phenotype of  Tgfbr2  conditional knockout mice. In summary, our results reveal the functional similarity between TGFBR2 and TGFBR1 in maintaining the structural integrity of the female reproductive tract.

Functional similarity between TGF-beta type 2 and type 1 receptors in the female reproductive tract