Fig 1: Experiments in Tg mice and WT controls. Standard histology of testis (a–d) shows no difference in number, size, and cellular compound of seminiferous tubules between Tg mice and control. Diameter (e), and thickness (f) of 100 seminiferous tubules per mouse were measured: histograms show mean and standard deviation, no significant difference was found; (g) testis weight; (h) sperm count; (i,j) protein and mRNA levels of Dyrk1A in testis and brain; (k,f,l) IHC assay for Dyrk1A in the testis of Tg mice and WT controls. The two groups of mice did not differ in the number and intensity of Dyrk1a+ cells in seminiferous tubules. In control mice, Dyrk1a was expressed by cells close to the basal membrane, corresponding to the early stages of spermatogenesis and as show in the cropped images: double arrowheads: small cells close to the basal membrane, corresponding to spermatogonia; single arrowheads: large cells not in contact with the basal membrane, corresponding to primary spermatocytes; square brackets: later stages of spermatogenesis, with a lower Dyrk1a intensity. p value : 0.033 (*), 0.002 (**), <0.001 (***).
Fig 2: Mechanisms of impaired fertility in Tg mice overexpressing DYRK1A. Hypogonadotropic hypogonadism (a) might be induced by central overexpression of DYRK1A in the hypothalamus and/or the pituitary; the overexpression might be responsible for lowering the production of LH and FSH gonadotrophins. In the testis, low LH levels slow down steroidogenesis and reduce testosterone levels, which in turn reduced spermatogenesis stimulation and upregulation of AMH levels in Sertoli cells. In germ cells (b), overexpression of DYRK1A in the early stages of spermatogenesis prompts spermatogonia to self-renew rather than to differentiate and enter meiosis. This process might be mediated by activation of STAT3 and GDNF, downregulation of retinoic acid (RA), and perturbation of the mitosis-to-meiosis transition by excess AMH.
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