Localization of myosin in the preimplantation mouse embryo

Sobel, J. S.

doi:10.1016/0012-1606(83)90021-0

Cited by 48 publications

(13 citation statements)

References 15 publications

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“…Calmodulin also was regionalized in the areas opposite to cell contacts of compacted morulae. The same location has been reported for myosin (35,74). Inhibition of calmodulin with TFP induced its delocalization whereas morulae decompacted and [Ca 2ϩ ] i rose.…”

Section: Discussionsupporting

confidence: 56%

Increase of intracellular Ca ²⁺ and relocation of E-cadherin during experimental decompaction of mouse embryos

Pey

Vial

Schatten

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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To determine the role of intracellular Ca 2؉ in compaction, the first morphogenetic event in embryogenesis, we analyzed preimplantation mouse embryos under several decompacting conditions, including depletion of extracellular Ca 2؉ , blocking of Ca 2؉ channels, and inhibition of microfilaments, calmodulin, and intracellular Ca 2؉ release. Those treatments induced decompaction of mouse morulae and simultaneously induced changes in cytosolic free Ca 2؉ concentration and deregionalization of E-cadherin and fodrin. When morulae were allowed to recompact, the location of both proteins recovered. In contrast, actin did not change its cortical location with compaction nor with decompaction-recompaction. Calmodulin localized in areas opposite to cell-cell contacts in eight-cell stage embryos before and after compaction. Inhibition of calmodulin with trifluoperazine induced its delocalization while morulae decompacted. A nonspecific rise of intracellular free Ca 2؉ provoked by ionomycin did not affect the compacted shape. Moreover, the same decompacting treatments when applied to uncompacted embryos did not produce any change in intracellular Ca 2؉ . Our results demonstrate that in preimplantation mouse embryos experimentally induced stage-specific changes of cell shape are accompanied by changes of intracellular free Ca 2؉ and redistribution of the cytoskeleton-related proteins E-cadherin, fodrin, and calmodulin. We conclude that intracellular Ca 2؉ specifically is involved in compaction and probably regulates the function and localization of cytoskeleton elements.Extracellular calcium is crucial during the preimplantation development of mammalian embryos because of its role in cell-cell adhesion (1-5). Intracellular free calcium ([Ca 2ϩ ] i ) plays a pivotal role in triggering early events related to fertilization, namely, oocyte maturation, cortical granule exocytosis, and egg activation (6-19). However, little is known about the role of [Ca 2ϩ ] i during the following steps of mammalian development. Indirect evidence for a regulatory role was provided in experiments where development of mouse embryos was delayed by treatments with calcium channel blockers or with an inhibitor of calmodulin (20). It was only recently that [Ca 2ϩ ] i changes were studied directly during early mouse development. An endogenous increase in Ca 2ϩ -releasing activity leading to Ca 2ϩ transients was observed during the first mitotic division (21). Moreover, the rate of cavitation and cell division was either accelerated or delayed by experimentally induced elevation or reduction of [Ca 2ϩ ] i , respectively (22-24). Stacheki and Armant (24) suggested that in mouse embryos, inositol 1,4,5-trisphosphate-sensitive and ryanodinesensitive Ca 2ϩ stores exist at the morula stage and that calmodulin is involved in mediating the Ca 2ϩ signaling effects to its distal targets.Despite these temporal effects, no other developmental events have been examined so far under conditions where [Ca 2ϩ ] i has been manipulated and therefore t...

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Section: Discussionsupporting

confidence: 56%

Increase of intracellular Ca ²⁺ and relocation of E-cadherin during experimental decompaction of mouse embryos

Pey

Vial

Schatten

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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“…These data on the Par gene complex indicate that apical membrane PKCζ at compaction might contribute similarly to the process of early lineage diversification in the mouse embryo through cytoskeletal reorganization and cell polarity. Extensive cytoskeletal reorganization occurs during compaction and cell polarization in the embryo (Johnson and Maro, 1984;Maro and Pickering, 1984) with the submembraneous microvillous pole comprising actin and actin-binding proteins, including myosin (Sobel, 1983), tropomyosin (Clayton and Johnson, 1998) and ezrin (Louvet et al, 1996), as well as the TJ protein cingulin inherited from the oocyte . In addition to PKCζ polarisation, we found the novel PKCδ to concentrate at the apical surface pole of blastomeres at compaction.…”

Section: Discussionmentioning

confidence: 99%

Contribution of JAM-1 to epithelial differentiation and tight-junction biogenesis in the mouse preimplantation embryo

Thomas

Sheth

Eckert

et al. 2004

Journal of Cell Science

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We have investigated the contribution of the tight junction (TJ) transmembrane protein junction-adhesion-molecule 1 (JAM-1) to trophectoderm epithelial differentiation in the mouse embryo. JAM-1-encoding mRNA is expressed early from the embryonic genome and is detectable as protein from the eight-cell stage. Immunofluorescence confocal analysis of staged embryos and synchronized cell clusters revealed JAM-1 recruitment to cell contact sites occurred predominantly during the first hour after division to the eight-cell stage, earlier than any other TJ protein analysed to date in this model and before E-cadherin adhesion and cell polarization. During embryo compaction later in the fourth cell cycle, JAM-1 localized transiently yet precisely to the apical microvillous pole, where protein kinase Cζ (PKCζ) and PKCδ are also found, indicating a role in cell surface reorganization and polarization. Subsequently, in morulae and blastocysts, JAM-1 is distributed ubiquitously at cell contact sites within the embryo but is concentrated within the trophectoderm apicolateral junctional complex, a pattern resembling that of E-cadherin and nectin-2. However, treatment of embryos with anti-JAM-1-neutralizing antibodies indicated that JAM-1 did not contribute to global embryo compaction and adhesion but rather regulated the timing of blastocoel cavity formation dependent upon establishment of the trophectoderm TJ paracellular seal.

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“…Non-muscle cells do not need to generate forces equivalent to those in muscle cells as their requirement is restricted to processes within the cell itself such as cell division and locomotion [reviewed 16, 37, 391. Little is known about the function of non-muscle myosin in early embryonic development prior to the formation of muscle itself. In the mouse preimplantation embryo, myosin was detected in two-cell to morula stage embryos at the apical surfaces of the blastomeres after Triton X-100 extraction [32,33, reviewed 351. In the mouse preimplantation embryo, myosin was detected in two-cell to morula stage embryos at the apical surfaces of the blastomeres after Triton X-100 extraction [32,33, reviewed 351.…”

Section: Introductionmentioning

confidence: 99%

Organization of non-muscle myosin during early murine embryonic differentiation

et al. 1992

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Localization of myosin in the preimplantation mouse embryo

Cited by 48 publications

References 15 publications

Increase of intracellular Ca ²⁺ and relocation of E-cadherin during experimental decompaction of mouse embryos

Increase of intracellular Ca ²⁺ and relocation of E-cadherin during experimental decompaction of mouse embryos

Contribution of JAM-1 to epithelial differentiation and tight-junction biogenesis in the mouse preimplantation embryo

Organization of non-muscle myosin during early murine embryonic differentiation

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Localization of myosin in the preimplantation mouse embryo

Cited by 48 publications

References 15 publications

Increase of intracellular Ca 2+ and relocation of E-cadherin during experimental decompaction of mouse embryos

Increase of intracellular Ca 2+ and relocation of E-cadherin during experimental decompaction of mouse embryos

Contribution of JAM-1 to epithelial differentiation and tight-junction biogenesis in the mouse preimplantation embryo

Organization of non-muscle myosin during early murine embryonic differentiation

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Increase of intracellular Ca ²⁺ and relocation of E-cadherin during experimental decompaction of mouse embryos

Increase of intracellular Ca ²⁺ and relocation of E-cadherin during experimental decompaction of mouse embryos