Embryonic mortality in cattle from the embryo's perspective

ABSTRACT For the embryo to successfully complete development it must be capable of executing its developmental program within a microenvironment largely established by the mother. Mortality results either because of intrinsic defects within the embryo, an inadequate maternal environment, asynchrony between embryo and mother, or failure of the mother to respond appropriately to embryonic signals. To some extent, the embryo's fate is dictated by events before fertilization: embryos formed from incompetent oocytes have a low probability of successful development. For example, embryos have reduced developmental competence when formed from oocytes from persistent ovarian follicles or from cows during the summer in Florida. Chromosomal abnormalities, caused by incompetent gametes or other causes, and homozygous recessive genes, exacerbated by inbreeding, represent additional types of intrinsic errors responsible for embryonic loss. Alterations in the maternal environment can cause embryonic mortality, as has been shown for heat stress and feeding diets high in degradable protein. The preimplantation embryo is most susceptible to certain types of stresses (most notably, heat shock) very early in development when its genome is largely repressed. Thus, the cellular adjustments the early embryo can make in response to perturbations in its environment are limited. Some genes related to resistance to cellular stress can become activated early in development (for example, heat shock protein 70) while other responses to stress are absent. For example, the early bovine embryo cannot undergo apoptosis in response to cellular stresses that ordinarily activate this process. One possibility is that the acquisition of the capacity for apoptosis represents an important mechanism by which an embryo acquires the ability to survive cellular stress. The embryo can also modify, to some extent, an inappropriate maternal environment. Development of procedures to improve oocyte competence and to manipulate embryonic stress responses may lead to new practices for improving embryonic survival.

Implications

Pregnancy rate per insemination in dairy cattle has declined in the last 30 yr or so in the United States and Great Britain (Royal et al., 2000; Lucy, 2001). Although some of this decline likely reflects failures of estrus detection, improper semen deposition, and so on, such a large decrease in pregnancy rate points to an increase in embryonic mortality. Evidence gathered in this review indicates that one source of embryonic mortality is inadequate oocyte growth and maturation leading to an oocyte that is incapable of becoming a healthy embryo. Perhaps failure of the embryo to undergo cellular adaptations to stabilize embryonic function in the face of an adverse maternal environment is another source of embryonic loss. Research directed toward improving oocyte competence and toward manipulation of embryonic stress responses may lead to new methods for enhancing fertility in cattle and other species.

Key Words: Development, Embryos, Fertility, Mortality, Oocytes

© 2002 American Society of Animal Science. All rights reserved.
J. Anim. Sci. 80(E. Suppl. 2):E33-E44