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Specific PKC isoforms regulate blastocoel formation during mouse preimplantation development preimplantation development

Specific PKC isoforms regulate blastocoel formation during mouse preimplantation development preimplantation development
Specific PKC isoforms regulate blastocoel formation during mouse preimplantation development preimplantation development
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 blastocystmorphogenesis. Specific inhibition of PKCy and ~ activity significantly delayed blastocyst formation. Although modulation of these PKCisoforms 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.
protein kinase C, mouse embryo, blastocyst, trophectoderm, inner cell mass, tight junction, ZO-1, Na+/K+ ATPase, cavitation
0012-1606
384-401
Eckert, Judith J.
729bfa49-7053-458d-8e84-3e70e4d98e57
McCallum, Amanda
13df1cf2-9b9d-47fc-a184-1f768d429672
Mears, Andrew
36c51693-c476-4f3f-a5a0-bc18b935e38f
Rumsby, Martin G.
ffedf189-2943-4a8d-9b75-bcfb9fa8323c
Cameron, Iain T.
f7595539-efa6-4687-b161-e1e93ff710f2
Fleming, Tom P.
2abf761a-e5a1-4fa7-a2c8-12e32d5d4c03
Eckert, Judith J.
729bfa49-7053-458d-8e84-3e70e4d98e57
McCallum, Amanda
13df1cf2-9b9d-47fc-a184-1f768d429672
Mears, Andrew
36c51693-c476-4f3f-a5a0-bc18b935e38f
Rumsby, Martin G.
ffedf189-2943-4a8d-9b75-bcfb9fa8323c
Cameron, Iain T.
f7595539-efa6-4687-b161-e1e93ff710f2
Fleming, Tom P.
2abf761a-e5a1-4fa7-a2c8-12e32d5d4c03

Eckert, Judith J., McCallum, Amanda, Mears, Andrew, Rumsby, Martin G., Cameron, Iain T. and Fleming, Tom P. (2004) Specific PKC isoforms regulate blastocoel formation during mouse preimplantation development preimplantation development. Developmental Biology, 274 (2), 384-401. (doi:10.1016/j.ydbio.2004.07.027).

Record type: Article

Abstract

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 blastocystmorphogenesis. Specific inhibition of PKCy and ~ activity significantly delayed blastocyst formation. Although modulation of these PKCisoforms 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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Submitted date: 20 May 2004
Published date: 15 October 2004
Keywords: protein kinase C, mouse embryo, blastocyst, trophectoderm, inner cell mass, tight junction, ZO-1, Na+/K+ ATPase, cavitation

Identifiers

Local EPrints ID: 24227
URI: http://eprints.soton.ac.uk/id/eprint/24227
ISSN: 0012-1606
PURE UUID: 470ba679-d4de-421e-b1c2-ee3d6ea2c28c
ORCID for Iain T. Cameron: ORCID iD orcid.org/0000-0002-4875-267X

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Date deposited: 29 Mar 2006
Last modified: 28 Apr 2022 01:43

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Contributors

Author: Amanda McCallum
Author: Andrew Mears
Author: Martin G. Rumsby
Author: Iain T. Cameron ORCID iD
Author: Tom P. Fleming

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