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J Cell Biol. 2017 May 1;216(5):1387-1404. doi: 10.1083/jcb.201608038. Epub 2017 Mar 31.

Myosin II promotes the anisotropic loss of the apical domain during Drosophila neuroblast ingression.

Author information

1
Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
2
Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario M5S 1M1, Canada.
3
Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada u.tepass@utoronto.ca.

Abstract

Epithelial-mesenchymal transitions play key roles in development and cancer and entail the loss of epithelial polarity and cell adhesion. In this study, we use quantitative live imaging of ingressing neuroblasts (NBs) in Drosophila melanogaster embryos to assess apical domain loss and junctional disassembly. Ingression is independent of the Snail family of transcriptional repressors and down-regulation of Drosophila E-cadherin (DEcad) transcription. Instead, the posttranscriptionally regulated decrease in DEcad coincides with the reduction of cell contact length and depends on tension anisotropy between NBs and their neighbors. A major driver of apical constriction and junctional disassembly are periodic pulses of junctional and medial myosin II that result in progressively stronger cortical contractions during ingression. Effective contractions require the molecular coupling between myosin and junctions and apical relaxation of neighboring cells. Moreover, planar polarization of myosin leads to the loss of anterior-posterior junctions before the loss of dorsal-ventral junctions. We conclude that planar-polarized dynamic actomyosin networks drive apical constriction and the anisotropic loss of cell contacts during NB ingression.

PMID:
28363972
PMCID:
PMC5412560
DOI:
10.1083/jcb.201608038
[Indexed for MEDLINE]
Free PMC Article

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