Figure 1.
Sdk controls epithelial remodeling and fluctuations of cell contact length. (Refers to Videos 1 and 2 and Table S1.) (A) Left: Schematics of major steps in lattice remodeling. Right: Types of LCs, periods of expansion and contraction of LC–LC contacts, and contracted or expanded cell–cell contacts in this and subsequent figures. (B) Sdk consists of 6 immunoglobulin (Ig) domains, 13 Fibronectin type III domains (FN3), a transmembrane (TM) domain and a predicted WIRS motif. (C–H) Cellular defects in sdk mutants and HA::Sdk-expressing eyes compared with WT. (C) WT; each bristle cell, and 3° LC, connects to three 2° LCs as in colored overlay. (D)sdk mutant; common defects include cellular rosettes (magenta), missing LCs (blue), and extra LCs (brown; Fig. S1). (E)sdk mutant clones; cellular rosettes can consist of mutant and/or WT cells, see quantification in H. (F) GMR>HA::Sdk; LC–LC contacts are lost and replaced with 1°–1° contacts (white arrowheads) and large elongated vesicles persist at the cell surface (yellow arrowhead). (G) Quantification of the frequency of ommatidia vertices associated with intercalation defects and the frequency of edges associated with extra cells or missing cells and misplaced bristles in sdk mutants and GMR>HA::Sdk eyes compared with WT. χ2 test; ***, P < 0.001. (H) Quantification of the mutant and WT cell composition in 39 rosettes in 5 eyes containing sdk MARCM clones. (I–L) Cellular and contact dynamics in sdk mutant and GMR>HA::Sdk eyes compared with WT, 26–28 h APF (Video 1). (I) WT; contacts expand and contract cyclically. (J)sdk mutants; a subset of contacts transiently separate. (K) GMR>HA::Sdk; contacts separate either transiently or permanently. (L) Quantification of the amplitude of contact expansion and frequency of contact pulsing along horizontal edges. WT, n = 20 contacts in two retinas; sdkMB05054, n = 20 contacts in two retinas; sdkΔ15, n = 30 contacts in three retinas; GMR>HA::Sdk, n = 20 contacts in two retinas. Kruskal–Wallis test with Dunn’s multiple comparison test for pulse amplitudes, overall P < 0.0001; sdkΔ15 versus WT, P = 0.0189; sdkMB05054 versus WT, P = 0.0037; GMR>Sdk::HA versus WT, P < 0.0001, for pulse frequencies, overall P = .0923, sdkΔ15 vs. WT P > .9999, sdkMB05054 vs. WT P = .3918, GMR>HA::Sdk vs. WT P = .1341. (M) WT; vesicles bud from cone–1° contacts and move to 1°–LC contacts. Arrowheads trace vesicle movement. (N) GMR>HA::Sdk causes a delay of vesicle budding and their enlargement to form tubules. Arrowhead traces a vesicle arrested at budding (Video 2). (O) GMR>HA::Sdk expression in Sdk::GFP eyes. 36 h APF; HA::Sdk is broadly distributed along cell contacts and is excluded from vertices at this and earlier stages. Scale bar, 5 μm.

Sdk controls epithelial remodeling and fluctuations of cell contact length. (Refers to Videos 1 and 2 and Table S1.) (A) Left: Schematics of major steps in lattice remodeling. Right: Types of LCs, periods of expansion and contraction of LC–LC contacts, and contracted or expanded cell–cell contacts in this and subsequent figures. (B) Sdk consists of 6 immunoglobulin (Ig) domains, 13 Fibronectin type III domains (FN3), a transmembrane (TM) domain and a predicted WIRS motif. (C–H) Cellular defects in sdk mutants and HA::Sdk-expressing eyes compared with WT. (C) WT; each bristle cell, and 3° LC, connects to three 2° LCs as in colored overlay. (D)sdk mutant; common defects include cellular rosettes (magenta), missing LCs (blue), and extra LCs (brown; Fig. S1). (E)sdk mutant clones; cellular rosettes can consist of mutant and/or WT cells, see quantification in H. (F) GMR>HA::Sdk; LC–LC contacts are lost and replaced with 1°–1° contacts (white arrowheads) and large elongated vesicles persist at the cell surface (yellow arrowhead). (G) Quantification of the frequency of ommatidia vertices associated with intercalation defects and the frequency of edges associated with extra cells or missing cells and misplaced bristles in sdk mutants and GMR>HA::Sdk eyes compared with WT. χ2 test; ***, P < 0.001. (H) Quantification of the mutant and WT cell composition in 39 rosettes in 5 eyes containing sdk MARCM clones. (I–L) Cellular and contact dynamics in sdk mutant and GMR>HA::Sdk eyes compared with WT, 26–28 h APF (Video 1). (I) WT; contacts expand and contract cyclically. (J)sdk mutants; a subset of contacts transiently separate. (K) GMR>HA::Sdk; contacts separate either transiently or permanently. (L) Quantification of the amplitude of contact expansion and frequency of contact pulsing along horizontal edges. WT, n = 20 contacts in two retinas; sdkMB05054, n = 20 contacts in two retinas; sdkΔ15, n = 30 contacts in three retinas; GMR>HA::Sdk, n = 20 contacts in two retinas. Kruskal–Wallis test with Dunn’s multiple comparison test for pulse amplitudes, overall P < 0.0001; sdkΔ15 versus WT, P = 0.0189; sdkMB05054 versus WT, P = 0.0037; GMR>Sdk::HA versus WT, P < 0.0001, for pulse frequencies, overall P = .0923, sdkΔ15 vs. WT P > .9999, sdkMB05054 vs. WT P = .3918, GMR>HA::Sdk vs. WT P = .1341. (M) WT; vesicles bud from cone–1° contacts and move to 1°–LC contacts. Arrowheads trace vesicle movement. (N) GMR>HA::Sdk causes a delay of vesicle budding and their enlargement to form tubules. Arrowhead traces a vesicle arrested at budding (Video 2). (O) GMR>HA::Sdk expression in Sdk::GFP eyes. 36 h APF; HA::Sdk is broadly distributed along cell contacts and is excluded from vertices at this and earlier stages. Scale bar, 5 μm.

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