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In Mammals, structural rearrangements of the karyotype cause considerable trouble to the spermatogenic process. Making use of an experimental animal model of Robertsonian chromosomal variation in the house mouse (Gropp, Winking &amp; Redi, 1982a) the effects of these chromosome structural rearrangements on the spermatogenic process were studied in fertile and chromosomally derived subfertile and sterile mice. Each karyotype condition was related to the cytological composition of the twelve stages of the seminiferous epithelium, studied in PAS-haematoxylin-stained testicular sections, with the following results: 1) in subfertile males there is a depletion of spermatogonia in the regenerating compartment but their differentiation is not affected. In the sterile males there is degeneration of primary and secondary spermatocytes and massive spermatid degeneration. 2) Spermatocyte development is retarded in nearly 50 % of the spermatocyte population in subfertile males. Moreover the ratio between primary spermatocytes and spermatids is reduced to about 1:2 in subfertile males, while the few spermatids produced in sterile males had degenerated during stages I to VIII. 3) The number of Sertoli cells/100 μm throughout the cycle of spermatogenesis is the same in the three conditions studied. These data indicate that the spermatogenic process is affected by structural changes not only at the meiotic level (primary spermatocyte failure to follow the normal pattern of differentiation and occurrence of defective spermatids) but also at the premeiotic stage, when undifferentiated spermatogonia are regenerating.

The effects of some Robertsonian chromosome combinations on the seminiferous epithelium of the mouse