Biology subjects

Fuentes, M. A.

Publications and source records attributed to Fuentes, M. A..

2 recordsLinked to original sources

bioRxiv2022

Dlg1 regulates subcellular distribution of non-muscle myosin II during Drosophila germband extension

Elongation 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.

developmental biology↗

bioRxiv2021

Cell polarity determinant Dlg1 facilitates epithelial invagination by promoting tissue-scale mechanical coordination

Epithelial folding mediated by apical constriction serves as a fundamental mechanism to convert flat epithelial sheets into multilayered structures. It remains elusive whether additional mechanical inputs are required for folding mediated by apical constriction. Using Drosophila mesoderm invagination as a model, we identified an important role for the non-constricting, lateral mesodermal cells adjacent to the constriction domain ("flanking cells") in facilitating epithelial folding. We found that depletion of the basolateral determinant, Dlg1, disrupts the transition between apical constriction and invagination without affecting the rate of apical constriction. Strikingly, the observed delay in invagination is associated with ineffective apical myosin contractions in the flanking cells that lead to overstretching of their apical domain. The defects in the flanking cells impede ventral-directed movement of the lateral ectoderm, suggesting reduced mechanical coupling between tissues. Specifically disrupting the flanking cells in wildtype embryos by laser ablation or optogenetic depletion of cortical actin is sufficient to delay the apical constriction-to-invagination transition. Our findings indicate that effective mesoderm invagination requires intact flanking cells and suggest a role for tissue-scale mechanical coupling during epithelial folding.

developmental biology↗