Fig 6.

Heightened STAT92E signaling contributes to the female fecundity defect in PTP61FΔ mutant flies. (A) Protein extracts from ovarian tissue were immunoblotted with antibodies against the phosphorylated and activated forms of STAT (p-STAT92E) and the IR (p-IR). p-IR is increased in the ovaries of PTP61FΔ homozygous mutants. p-STAT92E is increased in both PTP61FΔ homozygotes and heterozygotes. Results shown are representative of at least 2 or 3 independent experiments. (B and C) Fecundity assays were performed using single-pair matings of females of the indicated genotype with w¹¹¹⁸ males. Results are means ± SEM; n = 8 to 10. **, P < 0.01. (B) Reducing PI3K signaling in the PTP61FΔ mutant background by overexpressing dominant negative dp110 (dp110DN) using the arm-Gal4 driver did not restore fecundity (P = 0.36). Control, arm>dp110DN; PTP61FΔ/+. (C) Suppression of STAT92E in the PTP61FΔ homozygous background using in vivo RNAi (STATRNAi) resulted in a partial rescue of fecundity. Control, arm>STATRNAi; PTP61FΔ/+.