Abstract
Embryonic diapause is an evolutionary strategy by which a reversible arrest in embryo development occurs. In its two forms, facultative and obligate, it assures that offspring are born when optimal maternal and environmental conditions are present to ensure maximal survival. We have explored obligate delayed implantation in the mink over four decades, first by evaluation of the environmental regulation, then by determination of the pituitary factors that maintain diapause and provoke implantation followed by evaluation of the ovarian contribution to the process. As the uterine environment is the proximal regulator of diapause, we employed a strategy of global gene analysis to discover differentially expressed pathways during embryo arrest and reactivation. These trials revealed that the synthesis of polyamines was increased in the uterus with reactivation of the embryo in vivo. Subsequent experiments demonstrated that the polyamine, putrescine, was capable of inducing escape of the embryo from obligate diapause, providing strong evidence that the paucity of polyamines induces developmental arrest and reactivation is coupled to renewed uterine and/embryonic synthesis of these polycations.
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References
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Acknowledgements
All of the original research on obligate diapause in my laboratory has been supported by the generous and continuous support of the Natural Sciences and Engineering Research Council of Canada. A number of talented students and postdoctoral fellows, dedicated technicians, undergraduate research students and colleagues participated in these investigations, and I gratefully acknowledge their invaluable contributions.
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Murphy, B.D. (2012). Resolving the enigma of embryonic diapause, a forty-year scientific journey. In: Larsen, P.F., et al. Proceedings of the Xth International Scientific Congress in fur animal production. Wageningen Academic Publishers, Wageningen. https://doi.org/10.3920/978-90-8686-760-8_33
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DOI: https://doi.org/10.3920/978-90-8686-760-8_33
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