imprint:
Proceedings of the National Academy of Sciences, 1998
Published in:Proceedings of the National Academy of Sciences
Language:
English
DOI:
10.1073/pnas.95.22.12977
ISSN:
0027-8424;
1091-6490
Origination:
Footnote:
Description:
<jats:p>
To determine the role of intracellular Ca
<jats:sup>2+</jats:sup>
in compaction, the first morphogenetic event in embryogenesis, we analyzed preimplantation mouse embryos under several decompacting conditions, including depletion of extracellular Ca
<jats:sup>2+</jats:sup>
, blocking of Ca
<jats:sup>2+</jats:sup>
channels, and inhibition of microfilaments, calmodulin, and intracellular Ca
<jats:sup>2+</jats:sup>
release. Those treatments induced decompaction of mouse morulae and simultaneously induced changes in cytosolic free Ca
<jats:sup>2+</jats:sup>
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
<jats:sup>2+</jats:sup>
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
<jats:sup>2+</jats:sup>
. Our results demonstrate that in preimplantation mouse embryos experimentally induced stage-specific changes of cell shape are accompanied by changes of intracellular free Ca
<jats:sup>2+</jats:sup>
and redistribution of the cytoskeleton-related proteins E-cadherin, fodrin, and calmodulin. We conclude that intracellular Ca
<jats:sup>2+</jats:sup>
specifically is involved in compaction and probably regulates the function and localization of cytoskeleton elements.
</jats:p>