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J Cell Biol. 2016 Jan 18;212(2):219-29. doi: 10.1083/jcb.201508056. Epub 2016 Jan 11.

Myosin-dependent remodeling of adherens junctions protects junctions from Snail-dependent disassembly.

Author information

1
Department of Molecular Biology, Princeton University, Princeton, NJ 08540 Howard Hughes Medical Institute, Princeton University, Princeton, NJ 08540.
2
Department of Molecular Biology, Princeton University, Princeton, NJ 08540 Howard Hughes Medical Institute, Princeton University, Princeton, NJ 08540 efw@princeton.edu.

Abstract

Although Snail is essential for disassembly of adherens junctions during epithelial-mesenchymal transitions (EMTs), loss of adherens junctions in Drosophila melanogaster gastrula is delayed until mesoderm is internalized, despite the early expression of Snail in that primordium. By combining live imaging and quantitative image analysis, we track the behavior of E-cadherin-rich junction clusters, demonstrating that in the early stages of gastrulation most subapical clusters in mesoderm not only persist, but move apically and enhance in density and total intensity. All three phenomena depend on myosin II and are temporally correlated with the pulses of actomyosin accumulation that drive initial cell shape changes during gastrulation. When contractile myosin is absent, the normal Snail expression in mesoderm, or ectopic Snail expression in ectoderm, is sufficient to drive early disassembly of junctions. In both cases, junctional disassembly can be blocked by simultaneous induction of myosin contractility. Our findings provide in vivo evidence for mechanosensitivity of cell-cell junctions and imply that myosin-mediated tension can prevent Snail-driven EMT.

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PMID:
26754645
PMCID:
PMC4738385
DOI:
10.1083/jcb.201508056
[Indexed for MEDLINE]
Free PMC Article

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