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. Author manuscript; available in PMC: 2014 Sep 23.
Published in final edited form as: Curr Biol. 2013 Sep 5;23(18):10.1016/j.cub.2013.07.054. doi: 10.1016/j.cub.2013.07.054

Figure 4. Pico/RIAM functions upstream of talin autoinhibition during morphogenesis.

Figure 4

(A) Schematic diagram of RIAM30-CAAX (B) WT embryos and embryos expressing RIAM30-CAAX in the AS were scored for openings in the dorsal epidermis at stage 13–17. (C) Stage 15 embryo with an open dorsal hole (arrowhead) stained for amnioserosa (green), integrin (red), and F-actin (blue). (D-E) The recruitment of talinGFP (D) and talinGFP*E1777A (E) to MTJs in control embryos and embryos expressing RIAM30-CAAX. (F) To provide evidence of pico knockdown based on the previously described pico phenotype [34], we measured adult body size of control embryos and embryos expressing picoRNAi under the control of a ubiquitous driver. (G-J) FRAP experiments were performed on talinGFP (G,H) and talinGFP*E1777A (I,J) to determine the effect of expressing either RIAM30-CAAX (G,I) or picoRNAi (H,J) on the mobility of talin at MTJs. (M) Model for the role and regulation of talin autoinhibition. RIAM-Rap1 acts to localize autoinhibited talin to integrin-mediated adhesions where autoinhibition can be relieved by electrostatic membrane interactions. This mechanism promotes stable adhesion, thus down-regulating cell motility required for morphogenesis.