Abstract
Maintaining lineage restriction boundaries in proliferating tissues is vital to animal development. A long-standing thermodynamics theory, the differential adhesion hypothesis, attributes cell sorting phenomena to differentially expressed adhesion molecules. However, the contribution of the differential adhesion system during tissue morphogenesis has been unsubstantiated despite substantial theoretical support. Here, we report that Toll-1, a transmembrane receptor protein, acts as a differentially expressed adhesion molecule that straightens the fluctuating anteroposterior compartment boundary in the abdominal epidermal epithelium of the Drosophila pupa. Toll-1 is expressed across the entire posterior compartment under the control of the selector gene engrailed and displays a sharp expression boundary that coincides with the compartment boundary. Toll-1 corrects local distortions of the boundary in the absence of cable-like Myosin II enrichment along the boundary. The reinforced adhesion of homotypic cell contacts, together with pulsed cell contraction, achieves a biased vertex sliding action by resisting the separation of homotypic cell contacts in boundary cells. This work reveals a self-organizing system that integrates a differential adhesion system with pulsed contraction of cells to maintain lineage restriction boundaries.
Highlights
Maintaining lineage restriction boundaries in proliferating tissues is vital to animal development
The signaling events that maintain boundaries during epithelial tissue morphogenesis have been intensively studied in the developmental compartments of Drosophila[3,4,5,6,7,8]
It has been shown in Drosophila tissues that local increases in mechanical tension on cell junctions along the compartment boundaries counteract the mechanical challenges caused by cell proliferation and rearrangement[13,14,15]
Summary
Sharp expression boundary of Toll-1 at the compartment boundary is established by engrailed. The vertices at the AP boundary were displaced significantly less than when the cell would undergo isotropic cell shape change during expansion phases (Fig. 5d–f) This outward displacement bias was abolished in the Tl knockdown tissues, suggesting that the Tl trans homophilic adhesions resist the sliding of vertices that would otherwise cause the separation of homotypic cell–cell contacts (Fig. 5e, f). Inward vertex displacements at the AP boundary were comparable to those of isotropic cell shape change during the contraction phase, both in control and Tl knockdown (Fig. 5f) These results suggest that the adhesion mediated by Tl contributes to extending the homotypic cell–cell contacts between P cells by resisting the separation of these junctions
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