Eckert, Judith J., McCallum, Amanda, Mears, Andrew, Rumsby, Martin G., Cameron, Iain T. and Fleming, Tom P.
Specific PKC isoforms regulate blastocoel formation during mouse preimplantation developmentpreimplantation development
Developmental Biology, 274, (2), . (doi:10.1016/j.ydbio.2004.07.027).
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During early mammalian development, blastocyst morphogenesis is achieved by epithelial differentiation of trophectoderm (TE) and its
segregation from the inner cell mass (ICM). Two major interrelated features of TE differentiation required for blastocoel formation include
intercellular junction biogenesis and a directed ion transport system, mediated by Na+/K+ ATPase. We have examined the relative
contribution of intercellular signalling mediated by protein kinase C (PKC) and gap junctional communication in TE differentiation and
blastocyst cavitation. The distribution pattern of four (y, u, L/E, ~) PKC isoforms and PKCA/PKD1 showed partial colocalisation with the tight
junction marker ZO-1a+ in TE and all four PKCs (y, u, L/E, ~) showed distinct TE/ICM staining patterns (predominantly at the cell
membrane within the TE and cytoplasmic within the ICM), indicating their potential contribution to TE differentiation and blastocyst
morphogenesis. Specific inhibition of PKCy and ~ activity significantly delayed blastocyst formation. Although modulation of these PKC
isoforms failed to influence the already established programme of epithelial junctional differentiation within the TE, Na+/K+ ATPase a1
subunit was internalised from membrane to cytoplasm. Inhibition of gap junctional communication, in contrast, had no influence on any of
these processes. Our results demonstrate for the first time that distinct PKC isotypes contribute to the regulation of cavitation in
preimplantation embryos via target proteins including Na+/K+ ATPase.
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