Abstract
ABSTRACTEpithelial folding shapes embryos and tissues during development. Here, we investigate the coupling between epithelial folding and actomyosin-enriched compartmental boundaries. The mechanistic relationship between the two is unclear, because actomyosin-enriched boundaries are not necessarily associated with folds. Also, some cases of epithelial folding occur independently of actomyosin contractility. We investigated the shallow folds called parasegment grooves that form at boundaries between anterior and posterior compartments in the early Drosophila embryo. We demonstrate that formation of these folds requires the presence of an actomyosin enrichment along the boundary cell-cell contacts. These enrichments, which require Wingless signalling, increase interfacial tension not only at the level of the adherens junctions but also along the lateral surfaces. We find that epithelial folding is normally under inhibitory control because different genetic manipulations, including depletion of the Myosin II phosphatase Flapwing, increase the depth of folds at boundaries. Fold depth correlates with the levels of Bazooka (Baz), the Par-3 homologue, along the boundary cell-cell contacts. Moreover, Wingless and Hedgehog signalling have opposite effects on fold depth at the boundary that correlate with changes in Baz planar polarity.
Highlights
Epithelial sheet bending is essential to elaborate the anatomy of animal bodies
Epithelial folding at PSBs is independent of apical constriction or adherens junctions (AJs) lowering To understand better the mechanisms leading to folding at PSBs, we examined cell behaviours during both endogenous and ectopic fold formation in live embryos, for a period of 30 min (Fig. 6)
Actomyosin enrichment at PSBs is required for epithelial folding In this paper, we demonstrate that the formation of parasegmental grooves requires an actomyosin enrichment at PSBs
Summary
Epithelial sheet bending is essential to elaborate the anatomy of animal bodies. It is ubiquitous throughout development, from gastrulation to organogenesis (Bazin-Lopez et al, 2015; Keller and Shook, 2011). The mechanisms identified so far that promote epithelial sheet bending are diverse (Pearl et al, 2017). One of the best-studied mechanisms is apical constriction mediated by actomyosin activation at the apical end of epithelial cells (Martin and Goldstein, 2014). Received 24 May 2017; Accepted 9 March 2018 epithelial folding require actomyosin activity; a basal shift of the adherens junctions (AJs) is required instead for dorsal fold formation in Drosophila gastrulae (Wang et al, 2012)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
