Fig. 2

Exogenous gonadotrophin administration fails to reverse ovarian subfertility of APC2-deficient female mice. a APC2-deficiency caused a gene dose-dependent decrease in the number of ovulated COCs (mean ± SE) retrieved from the oviducts post-superovulation. b Upper panels, representative photomicrographs of retrieved COCs showing the presence of oocytes (black arrows) surrounded by cumulus cells (red arrows). Bar = 200 μm. Lower panels, oocytes freed from cumulus cells. Bar = 50 μm. c Average oocyte diameter (mean ± SE) among experimental groups, showing no difference. n = 4 for Apc2^+/+, n = 3 for Apc2^+/−, n = 5 for Apc2^−/−. Statistical significance between groups in panels a – c was determined using ANOVA test followed by LSD post hoc analysis (variances of experiment groups were homogeneous tested by Levene’s test). d, e Representative photomicrographs of (d) Apc2^+/+, and (e) Apc2^−/− superovulated ovaries, showing growing follicles (red arrows) and corpora lutea (black arrows). Bar = 500 μm. f, g Total number of (f) corpora lutea, and (g) healthy follicles counted across 100 serial sections of five superovulated stage-matched ovaries from different animals (mean ± SE; *P < 0.05, t-test). h Gene expression levels of hormone receptors by qRT-PCR on RNA extracted from whole ovaries of Apc2^+/+ and Apc2^−/− 10-week-old female mice. Relative expression levels are normalized to Actb expression. N = 4 except for lhcgr and Ar in Apc2^−/− where n = 3 (mean ± 95% confidence intervals; **P < 0.01, determined from confidence intervals) [45]