Abstract
AbstractElongation of the body axis through convergent extension is a conserved developmental process that is mediated by cell intercalation. During convergent extension of the germband epithelium in Drosophila embryos, planar polarized activation of non-muscle myosin II (“myosin”) promotes cell intercalation by facilitating patterned remodeling of adherens junctions. Here, we report that loss of the basolateral determinant Dlg1 leads to defects in the subcellular distribution of myosin during germband extension, and consequently, impairs proper junctional remodeling and apical area maintenance during cell intercalation. In dlg1 mutant embryos, ectopic accumulation of myosin is observed at the medioapical domain and along the lateral membrane, whereas junctional myosin is greatly reduced. Analogous myosin mis-localization patterns are observed upon knockdown of other basolateral determinants, Scrib and Lgl, but not the apical determinants. The function of Dlg1 in regulating the spatial distribution of myosin requires its intact SH3 and GUK domains and involves the Rho1 GEF Cyst, active Rho1 and Rok. We propose that Dlg1 facilitates correct junctional remodeling and prevents undesired apical area variation during cell intercalation by regulating the subcellular location of myosin activation.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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