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Department of Animal Sciences, University of Florida, Gainesville 32611-0910
1 Correspondence: PO Box 110910 (E-mail: Hansen{at}animal.ufl.edu).
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.
This article has been cited by other articles:
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  S L Rodriguez-Zas, K Schellander, and H A Lewin Biological interpretations of transcriptomic profiles in mammalian oocytes and embryos Reproduction, February 1, 2008; 135(2): 129 - 139. [Abstract] [Full Text] [PDF]
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Z. Roth and P.J. Hansen Sphingosine 1-Phosphate Protects Bovine Oocytes from Heat Shock During Maturation Biol Reprod, December 1, 2004; 71(6): 2072 - 2078. [Abstract] [Full Text] [PDF]
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