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Fig. 7. Overexpression of Fak56 downregulates integrin adhesion to the extracellular matrix without affecting linkage to the cytoskeleton. Muscles and their attachment sites in the epidermis are visualized in stage 16 embryos expressing either Fak56-GFP (A-F,M-P) or Fak56 (J-L) specifically in embryonic muscle, using the Mef2-GAL4 driver, or control embryos (G-I). (A-F) Embryos overexpressing Fak56-GFP specifically in muscle were stained with antibodies against {alpha}PS2 integrin (red) (A,B), or Talin (red) (D,E), or antiphospho-FAKPY397 (blue) (B). Fak56-GFP is localized at the muscle ends (C,F, arrows), and its overexpression causes loss of muscle adhesion, without affecting the initial localization of {alpha}PS2 integrin. However in muscles that detach, {alpha}PS2 integrin remains at the ends of the detached muscles (A,B, arrowheads) indicating its dissociation from the extracellular matrix. A similar effect on Talin localization is observed (D,E, arrowheads). (G-L) Embryos expressing ILK-GFP are shown probed with anti-myosin heavy chain (MHC, red), and the extracellular matrix component Tiggrin (blue) (I,L). In embryos overexpressing Fak56 (J-L), ILK-GFP and Tiggrin are localized at the muscle ends similar to controls (G-I). Embryos expressing Fak56-GFP analyzed with anti-{alpha}PS2 (red) and Tiggrin (blue) (M-P). In embryos overexpressing Fak56-GFP, Tiggrin can be seen at the attachment site (arrows), but is not particularly enriched at the ends of the detached muscles (arrowheads).