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. 2023 Jul 28;12:e84710. doi: 10.7554/eLife.84710

Figure 3. Mice with genetic manipulation of the PARL substrates PINK1, PGAM5, and TTC19 do not reproduce or modify Parl-/- testis phenotype.

(A) Immunoblots of testis mitochondria from 6-week-old WT and Parl−/− mice with antibodies for the established PARL substrates PINK1, PGAM5, TTC19, DIABLO, STARD7, and CLPB. Severe accumulation of unprocessed PINK1 and PGAM5, as well as severe decrease in the mature processed form of TTC19 are evident in Parl−/− testis. HSP60 is the loading control. (B) Histology of testes from 7-week-old mice of the indicated genotypes (HE stain, n = 3 for each genotype). Parl-/-/Pink1-/-, Parl-/-/Pgam5-/-, and Parl-/-/Pink1-/-/Pgam5-/- show complete lack of sperm production and no modification of the testicular phenotype compared to Parl-/- mice. Ttc19-/-, Pink1-/-, Pgam5-/-, and Pink1-/-/Pgam5-/- mice have no evident testis pathology and show normal sperm production (mature spermatozoa are indicated by asterisks), and are fertile. Scale bar, 145 µm.

Figure 3—source data 1. Original images for Figure 3A.

Figure 3.

Figure 3—figure supplement 1. Similar to what has been described in Parl-/- mice, immunohistochemistry for AIF-1 confirms spermatogenesis arrest with complete absence of spermatids in Parl-/-/Pink1-/-, Parl-/-/Pgam5-/-, and Parl-/-/Pink1-/-/Pgam5-/- mice.

Figure 3—figure supplement 1.

On the contrary, as observed in WT mice, normal seminiferous tubules in Pink1-/-, Pgam5-/-, Ttc19-/- and Pink1-/-/Pgam5-/- mice are populated by AIF-1-positive spermatids at different levels of maturation (n = 3 for each genotype).