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The severe degenerative phenomena that characterises spermatogenesis in mating blue sharks involves spatially separated germ cell and Sertoli cell apoptosis. Unlike that observed in multilayered type B spermatogonial and spermatocyte cysts caspase-3-depend entapoptosis of single and multinucleate type B spermatogonia in one to three spermatogonial layered cysts resulted in their complete fragmentation, delayed phagocytic removal and displacement of the apoptotic bodies towards the perilumenar Sertoli nuclei. Changes were observed in the immunostaining patterns of proliferating cell nuclear antigen (PCNA), including subtle changes in cytoplasmic and overall intense immunostaining, labelled single and multinucleate cell (MNC) apoptotic spermatogonial masses in premeiotic cysts indifferent stages of the protracted death process. Initial massive MNC formation at the mitosis–meiosis transition eventually left its imprint in the spermatogenic sequence in the form of vacuolated areas in the affected and subsequent stages. Some of the latter attempted further developmental advance but eventually degenerated. The observed higher PCNA index of spermatogonia in vacuolated testes compared to testes with the MNC type of degeneration indicated that the former testicular morphology represented, in essence, the recovery phase from the pronounced MNC death earlier. Events culminating in the eventual apoptotic demise of the Sertoli cells themselves included the abortion of further development (presumably due to a suboptimal Sertoli: germ cell ratio) of those germ cells left over from the wave of MNC death that swept the cysts. Eventually the Sertoli-cell-only cysts became apoptotic as they were engulfed by the infiltrating lymphomyeloid cells from the epigonal organ associated with the mature pole of the testis.

The caspase-dependent apoptosis gradient in the testis of the blue shark, Prionace glauca