Liu Di

Embryotropic actions of follistatin: paracrine and autocrine mediators of oocyte competence and embryo developmental progression

Despite several decades since the birth of the first test tube baby and the first calf derived from an in vitro-fertilised embryo, the efficiency of assisted reproductive technologies remains less than ideal. Poor oocyte competence is a major factor limiting the efficiency of in vitro embryo production. Developmental competence obtained during oocyte growth and maturation establishes the foundation for successful fertilisation and preimplantation embryonic development. Regulation of molecular and cellular events during fertilisation and embryo development is mediated, in part, by oocyte-derived factors acquired during oocyte growth and maturation and programmed by factors of follicular somatic cell origin. The available evidence supports an important intrinsic role for oocyte-derived follistatin and JY-1 proteins in mediating embryo developmental progression after fertilisation, and suggests that the paracrine and autocrine actions of oocyte-derived growth differentiation factor 9, bone morphogenetic protein 15 and follicular somatic cell-derived members of the fibroblast growth factor family impact oocyte competence and subsequent embryo developmental progression after fertilisation. An increased understanding of the molecular mechanisms mediating oocyte competence and stage-specific developmental events during early embryogenesis is crucial for further improvements in assisted reproductive technologies.

Effect of trichostatin A on transfected donor cells and subsequent development of porcine cloned embryos.

Transgenes integrated into mammalian cells are silenced rapidly. This phenomenon correlates with repressed chromatin structure marked by histone hypoacetylation. This study investigated the effect of trichostatin A (TSA; a histone-deacetylase inhibitor) on EGFP expression in transfected cells and embryonic development after somatic cell nuclear transfer (SCNT). Porcine adult fibroblasts were transfected with a pEGFP-C1 vector. Then transfected cells, donor cells for SCNT, were pretreated with TSA, with the untreated cells being used as the control. Expression of EGFP in donor cells and reconstructed embryos was detected when exposed to blue light. Results showed that the percentage of EGFP-positive cells significantly increased when the transfected cells were treated with TSA and the increased expression of EGFP was sustained to at least the morula stage. In addition, the cytotoxic effect of TSA on the transfected cells was dose dependent. In conclusion, TSA can rescue the silenced EGFP gene. Even after transferring the TSA-treated cells to enucleated recipient oocytes, TSA retained the ability to rescue a silenced EGFP gene. In addition, TSA had an impact on cell proliferation.