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Fig. 1. PKA mutant phenotypes and attempted rescue by constitutive PKA activity or LKB1. (A-D) PKA-C1 null germline clones do not prevent normal anterior migration of the oocyte nucleus (A, arrow), marked by orb-PZ expression in the germline nuclei (blue), normal expression of the dorsal follicle cell marker mirror^6D1 (B, purple), normal expression of the posterior follicle cell marker pnt^998/12 (C, red; green shows GFP-Stau mislocalized to the center of the oocyte, arrow) or normal expression of the centripetal follicle cell marker BB127 (D, blue). (E,F) Mislocalization of kin-ß-gal (green) and fusion of nurse cells, revealed by rhodamine-phalloidin staining of actin filaments (red), in PKA-C1 null germline clones (E). Both phenotypes are rescued by expression of the constitutively active mouse PKA catalytic subunit mC^* from an actin promoter (F). (G,H) GFP-Stau (green), like kin-ß-gal, is mislocalized toward the center of the oocyte in PKA-C1 null germline clones (G, arrow) and is restored to a normal posterior localization by expression of mC^* (H, arrow). Rhodamine-phalloidin (red) marks cell outlines. (I,J) Expression of the GFP-LKB1^S535E transgene (green) carrying a mutation that mimics phosphorylation at the putative PKA site does not perturb kin-ß-gal localization (red) in wild-type oocytes (I, arrow) but fails to rescue either kin-ß-gal mislocalization (red, arrow) or nurse cell fusions (outlined by GFP-LKB1^S535E in green) in PKA-C1 null germline clones (J).

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