Causes and consequences of early embryonic diversity in pigs.

Within 14 h of ovulation, follicular development in gilts was skewed towards a majority of mature follicles, based on their endocrine milieu. Oocyte maturation was also skewed, with a majority of the oocytes being meiotically more developed than the rest. Similarly, the pattern of ovulation in gilts was such that 70% of the follicles ovulated during a short period of time, while most of the remaining 30% ovulated over a more protracted period. This majority/minority pattern of both oocyte development and ovulation paralleled the distribution of development among 1-cell litter-mate embryos. Furthermore, oocytes of follicles predicted to ovulate first became the more developed embryos, while oocytes from later ovulating follicles became the lesser developed embryos. When these later ovulating follicles were destroyed by electrocautery, diversity in embryonic morphology was reduced by Day 12, and this reduction resulted from elimination of the lesser developed embryos. Genetic factors might also affect embryonic disparity, as SLA (swine leucocyte antigen complex) haplotype affected cleavage rates of embryos from miniature pigs. Results of various embryo transfer experiments demonstrated that the more developed embryos within a litter have a competitive advantage for survival over their less developed contemporaries. These lesser developed embryos, however, were just as viable as the more developed embryos after asynchronous transfer to recipients displaying onset of oestrus 1 day after the donors. The more developed embryos within the litter, by synthesizing more oestradiol than the smaller embryos, advanced uterine secretions. As a result, the lesser developed embryos probably became more susceptible to this new environment and eventually died in an asynchronous environment. Therefore, we suggest that early embryonic mortality directly relates to sequences of oocyte and follicular maturation, as oogenesis directs embryogenesis.