Fig. 2

HAT1 inhibition in GCs disturbs oocyte maturation. (A) Schematic illustration of in vitro maturation of COCs and DOs. (B) GVBD rate of COCs and DOs in the control (CTL) (COCs: n = 94, DOs: n = 116) and AA-treatment (AA) (COCs: n = 101, DOs: n = 123) groups. CTL: MEMα maturation medium with 40 µM DMSO; AA: MEMα maturation medium with 40 µM AA. (C) Left: Representative micrographs of PBE oocytes from COCs of the CTL and AA groups. Scale bar: 200 μm. Right: Quantification of the PBE rate of COCs and DOs in the CTL (COCs: n = 98, DOs: n = 113) and AA (COCs: n = 99, DOs: n = 118) groups. (D) The efficiency of siRNA (HAT1) in KGN cells by qRT‒PCR. The experiments were repeated three times independently with similar results. (E) Western blot analysis of the expression of HAT1 in the CTL and si-HAT1 group. The samples used to examine both the efficiency of si-HAT1 knockdown (Fig. 2E) and the level of apoptosis (Fig. 5A) were from the same batch of KGN cells, which leads to the same loading control. The experiments were repeated three times independently with similar results. (F) GVBD rate in the CTL (n = 74) and si-HAT1 (n = 77) groups. (G) Left: Representative micrographs of the PBE oocytes in the CTL and si-HAT1 groups. Scale bar: 200 μm. Right: Quantification of the PBE rate in the CTL (n = 69) and si-HAT1 (n = 74) groups. Data are presented as mean ± SEM, ns, no significance, *P < 0.05, **P < 0.01, ****P < 0.0001, Student’s t test