Regulation of diapause in carnivores
J C Fenelon1, P L Lefèvre1, A Banerjee1
1Centre de recherche en reproduction animale, Faculté de médecine vétérinare, Université de Montréal, St-Hyacinthe, QC, Canada.
Reproduction in Domestic Animals = Zuchthygiene
|December 28, 2016
Summary
Embryonic diapause in mustelids is regulated by pituitary prolactin, which controls uterine polyamine levels. Polyamines, specifically putrescine, are crucial for reactivating arrested embryos and terminating diapause.
Area of Science:
- Reproductive biology
- Developmental biology
- Carnivore genetics
Background:
- Embryonic diapause is an adaptive strategy for optimal offspring survival.
- Obligate embryonic diapause occurs in many carnivore species, regulated by photoperiod and pituitary prolactin.
- Uterine conditions are believed to cause embryonic arrest during diapause.
Purpose of the Study:
- To investigate the role of polyamines in embryonic diapause in mustelids.
- To identify the uterine factors responsible for maintaining embryonic arrest.
- To elucidate the mechanism by which pituitary prolactin influences embryonic development during diapause.
Main Methods:
- Global gene expression analysis in mink (Neovison vison) uteri during diapause.
- In vivo inhibition of polyamine synthesis (ornithine to putrescine).
- In vitro culture of mink embryos with varying concentrations of putrescine.
Main Results:
- Reduced expression of polyamine synthesis genes, including ornithine decarboxylase (ODC), was observed during diapause.
- Inhibition of putrescine synthesis induced reversible embryonic arrest and inhibited proliferation.
- Putrescine supplementation reactivated cultured mink embryos, indicated by increased embryo volume.
Conclusions:
- Pituitary prolactin regulates uterine polyamine synthesis via ODC1.
- Polyamines, particularly putrescine, are essential uterine factors for embryonic development.
- The absence of polyamines is the likely cause of embryonic diapause in mustelid carnivores.
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