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. 2019 Jan 23;5(1):eaau9780. doi: 10.1126/sciadv.aau9780

Fig. 2. Deletion of Spo16 led to massive germline loss and infertility in both males and females.

Fig. 2

(A) Schematic diagram of the CRISPR-Cas9 strategy to generate null allele for Spo16. Exons, sgRNA, and primers are indicated. The detailed sequence is shown in fig. S2D. Chr, chromosomes. (B) Genotyping results to distinguish the WT (+) allele and the null allele (−), which contains 19-bp insertion. Mk, DNA marker. (C) Representative image of testes derived from Spo16+/− and Spo16−/− males at the age of PD42. (D) Weights of testes derived from WT and Spo16−/− males at indicated ages. Numbers of testes analyzed (n) are indicated. Error bars indicate SEM. n.s., not significant. Dashed line shows the weight of the knockout testes at PD90. ***P < 0.001 by two-tailed Student’s t tests. (E) H&E staining results of paraffin-embedded testes from WT and Spo16−/− males. Stages of seminiferous tubules in control testes are indicated. Scale bar, 50 μm. (F) Morphology of Spo16+/− and Spo16−/− ovaries at PD42. (G) Immunohistochemistry (IHC) staining of MVH showing the oocytes in WT and Spo16−/− ovaries at E17.5 and PD1. Scale bar, 50 μm.