Skip to main content

Advertisement

Fig. 1 | Neural Development

Fig. 1

From: Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia

Fig. 1

Afadin is crucial for maintenance of adherens junctions but not tight junctions in the dorsal telencephalon. At E12.5, in both (a) control (Mllt4 fl/fl) and (b) mutant (Emx1-Cre; Mllt4 fl/fl), N-cadherin is concentrated at adherens junctions. c, d The localization of the tight junction protein ZO-1 is similar in the control and mutant as well. e-j Electron micrographs of the E12.5 neuroepithelium at low (e, f) and high magnification (g-j) in control (g, h) and mutant (i, j) reveal that cells bordered with intact adherens junctions (white arrowheads) present a primary cilium basal body (black arrowheads). Mutant cells with disrupted adherens junctions (i) lack a primary cilium near the ventricular surface. Immunogold labeling of Afadin (h and j, right panels, black dots designated by black arrows) shows its expression at adherens junctions in control. (AJ, Adherens junctions; PC, Primary cilium). At E13.5, N-cadherin localization is disrupted in mutant (l) compared to control (k). n Expression of ZO-1 is not disrupted when compared to control (m). o-r Electron micrographs of E13.5 neuroepithelial cells at low (o, p) and high magnification (q, r) in control (o, q) and mutant (p, r) show that absence of Afadin further disorganizes cell-cell contacts with absence of a primary cilium at the ventricular surface. Scale bars: 10 μm (a-d; k-n); 1 μm (e, f, o and p); 0.2 μm (g-j, q and r)

Back to article page