Fig 5.

PTP61FΔ mutant flies have reduced female fecundity due to increased apoptosis in developing egg chambers. (A) Fecundity assays were performed using single-pair matings of females of the indicated genotype. Fecundity assays separated by dashed lines were performed independently of each other. PTP61FΔ females have significantly decreased fecundity compared to w¹¹¹⁸ female controls (P = 9 × 10⁻⁵). When overexpressed together using arm-Gal4, PTP61Fm and PTP61Fn (arm>PTP61Fm+n) significantly rescued the fecundity defect of the PTP61FΔ mutant. PTP61Fm+n restored fecundity to a level not significantly different from that of control PTP61FΔ heterozygotes overexpressing PTP61Fm+n (P = 0.07). Overexpression of PTP61Fm or PTP61Fn individually in the PTP61FΔ mutant background resulted in only a partial rescue of fecundity, which was statistically different from what was observed in controls overexpressing the PTPs in the heterozygote background. Results are means ± standard errors of the means (SEM) for n = 8 to 10. **, P < 0.01; ***, P < 0.001. (B) Ovaries from w¹¹¹⁸ and PTP61FΔ females were visualized under bright field and also immunostained with anti-vasa antibodies to identify germ line cells in the ovary. Ovaries from PTP61FΔ mutant females lack later-stage egg chambers (post-stage 10) compared to controls. Results shown are representative of 3 experiments. (C) TUNEL staining of egg chambers (magnification, ×100) from PTP61FΔ homozygous and heterozygous female ovaries demonstrated that in the PTP61FΔ mutants there was an approximate 8-fold increase in the number of apoptotic pre-stage 10 egg chambers compared to PTP61FΔ heterozygotes. Results are means ± SEM for n = 8. **, P < 0.01.