Abstract
It has now been a decade since the first discovery of the intracellular Smad proteins, the downstream signalling molecules of one of the most important growth factor families in the animal kingdom, the transforming growth factor beta (TGF-beta) superfamily. In the ovary, several TGF-beta superfamily members are expressed by the oocyte, granulosa and thecal cells at different stages of folliculogenesis, and they signal mainly through two different Smad pathways in an autocrine/paracrine manner. Defects in the upstream signalling cascade molecules, the ligands and receptors, are known to have adverse effects on ovarian organogenesis and folliculogenesis, but the role of the individual Smad proteins in the proper function of the ovary is just beginning to be understood for example through the use of Smad knockout models. Although most of the different Smad knockouts are embryonic lethal, it is known, however, that in Smad1 and Smad5 knockout mice primordial germ cell development is impaired and that Smad3 deficient mice harbouring a deletion in exon 8 exhibit impaired folliculogenesis and reduced fertility. In this minireview we discuss the role of Smad structure and function in the ovarian context.
Highlights
The main function of the female ovary is the production of the mature oocyte for fertilization to allow subsequent generation of healthy progeny
Several growth factors belonging to the transforming growth factor β (TGFβ) superfamily together with their receptors and intracellular signalling molecules, the Smads, have been shown to be indispensable for the critical ovarian functions such as oocyte formation and development as well as ovarian folliculogenesis [1,2,3]
We focus on the role of the different Smads, the downstream effectors of TGF-β superfamily ligands, in the ovarian organogenesis and folliculogenesis
Summary
The main function of the female ovary is the production of the mature oocyte for fertilization to allow subsequent generation of healthy progeny. Defects at either the growth factor, receptor or intracellular effector level may abrogate proper signalling and lead to adverse effects in fertility as is shown by extensive knockout studies in mice (for reference see [1]) In this minireview, we focus on the role of the different Smads, the downstream effectors of TGF-β superfamily ligands, in the ovarian organogenesis and folliculogenesis. Reproductive defects can be found in knockout mice at all levels of the signalling cascade; at the ligand level activin β B, inhibin α, GDF-9, GDF-9B and AMH are known to cause fertility defects, at the receptor level, ALK6 ( known as BMP type IB receptor) and AMH type II receptor (AMHRII) affect female fertility, and at the intracellular effector level, Smad knockout mice exhibit reduced fertility [1,2,62].
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