Superresolution views of ZA remodeling in response to elevated contractility, and afadin’s role in this response. (A–D′, F, I, J″, L, and M) SIM of actomyosin and projections of apical 2-µm sections. (E–H, K, and N) EM, en face sections. (A–E) At BCJs, ZO KD cells assemble bundled actin cables decorated with periodic myosin structures absent in control—space between cables increases at TCJs (D, arrow). EM reveals periodic densities along BCJ cables (E, arrows). Myosin heavy chain antibodies plus MRLC-GFP reveal myosin minifilament polarity (F, arrows). (G and H) EM suggests that after ZO KD (H), actin cables spread apart as they reach TCJs (green arrows) and anchor end-on at junctions, leading to membrane folding (brackets and double arrows) not seen in control (G). (I–N) ZO/afadin KD. Actomyosin at BCJs (I, L [yellow arrows], J, and K) and some TCJs (arrowheads in I) is largely unchanged, but at many TCJs and MCJs, actin forms a more diffuse network, and periodic myosin structures expand laterally (I, L [magenta arrows], and M). Polarity of myosin minifilaments is unchanged (M, arrows). (N) EM reveals actin cables spread out and membrane remains folded near TCJs of ZO/afadin cells. Bars, 1 µm.