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RESEARCH ARTICLE

The requirement for protein kinase C delta (PRKCD) during preimplantation bovine embryo development

Qi-En Yang A B , Manabu Ozawa B D , Kun Zhang B E , Sally E. Johnson B C and Alan D. Ealy B C F
+ Author Affiliations
- Author Affiliations

A Key Laboratory of Adaption and Evolution of Plateau Biota, Northwest Plateau Institute of Biology, Chinese Academy of Sciences, Xining, Qinghai 810001, China.

B Department of Animal Sciences, University of Florida, Gainesville, FL 32611, USA.

C Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, 175 W. Campus Drive, Blacksburg, VA 24061, USA.

D Present address: Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.

E Present address: Department of Animal Science, Michigan State University, East Lansing, MI 48824-1225, USA.

F Corresponding author. Email: ealy@vt.edu

Reproduction, Fertility and Development 28(4) 482-490 https://doi.org/10.1071/RD14160
Submitted: 17 May 2014  Accepted: 17 July 2014   Published: 13 August 2014

Abstract

Protein kinase C (PKC) delta (PRKCD) is a member of the novel PKC subfamily that regulates gene expression in bovine trophoblast cells. Additional functions for PRKCD in early embryonic development in cattle have not been fully explored. The objectives of this study were to describe the expression profile of PRKCD mRNA in bovine embryos and to examine its biological roles during bovine embryo development. Both PRKCD mRNA and protein are present throughout early embryo development and increases in mRNA abundance are evident at morula and blastocyst stages. Phosphorylation patterns are consistent with detection of enzymatically active PRKCD in bovine embryos. Exposure to a pharmacological inhibitor (rottlerin) during early embryonic development prevented development beyond the eight- to 16-cell stage. Treatment at or after the 16-cell stage reduced blastocyst development rates, total blastomere numbers and inner cell mass-to-trophoblast cell ratio. Exposure to the inhibitor also decreased basal interferon tau (IFNT) transcript abundance and abolished fibroblast growth factor-2 induction of IFNT expression. Furthermore, trophoblast adhesion and proliferation was compromised in hatched blastocysts. These observations provide novel insights into PRKCD mRNA expression profiles in bovine embryos and provide evidence for PRKCD-dependent regulation of embryonic development, gene expression and post-hatching events.

Additional keywords: embryonic development, embryonic gene expression, post-hatching development.


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