Tyrphostin A9 improves blastocyst development in porcine embryos through induction of dynamin-related protein 1-dependent mitochondrial fission

- Tyrphostin A9 (TA9) improves the embryo development via regulating of Drp1-dependent mitochondrial fission in porcine.
- Mitochondrial fission-mediated apoptosis by high treatment of TA9 is reduced blastocyst development competence in porcine.
- Our results suggest a functional link between mitochondrial function and TA9 on early embryo development of porcine.
- Our study showed that regulation of mitochondrial appropriate fission by TA9 is required for embryo development in pigs.

Mitochondrial dynamics are associated with the development of porcine embryos. However, little is known about the effects of mitochondrial dynamics-related genes (Drp1 and pDrp1-Ser616) on early porcine embryo development. Here, we investigated the effect of Drp1-dependent mitochondrial fission signaling on the development of porcine embryos using the mitochondrial fission inducer, tyrphostin A9 (TA9). We determined that TA9 (1 μM) treated embryos were increased the mitochondrial functions, blastocyst development rate and quality, as well as decreased mitochondria-specific superoxide and mitochondrial apoptosis. Thus, TA9-induced appropriate mitochondrial fission improved the developmental competence via maintenance of a balance in mitochondrial dynamics in porcine embryo.