Y chromosomal fertility genes are essential for spermatogenesis, but those genes which code for major structural components of the spermatozoon and those controlling sperm morphogenesis must be located on a different chromosome. In the past, it had been questioned whether it would be possible to achieve a meaningful classification of male sterile mutations by light microscopy. I now show, however, that comparison of 244 autosomal male sterile mutants of Drosophila hydei with 400 similar mutants in D. melanogaster not only allows such a classification on the basis of the apparent targets, but also permits a genetic dissection of sperm morphogenesis. Differentiation of male germ cells is best characterized as spermeoteleosis, since male sterile mutations have the effect of aborting spermatogenesis rather than changing the cellular fate of the germ cells. In contrast to earlier proposals concerning sequential determinative events during this process, male sterile mutations can block spermatogenesis at nearly every stage, and not, as previously postulated, exclusively at the transitions between gonial, meiotic, and postmeiotic stages. Male sterile mutations can modify the topology of the organelles of a spermatid, and they can also affect the different components (i.e., nucleus, axoneme, nebenkern) of a germ cell to quite different degrees, leading to characteristic pleiotropic phenotypes. Some male sterile mutations can decouple the development of the different components of a germ cell, i.e., they may lead to a heterochrony of the development of the different subcellular structures, or they may permit the differentiation of some components of a germ cell even in the complete absence of an organelle. Thus, it is possible to describe spermatogenesis as the concerted, but not interdependent, execution of separate developmental programs for the particular components of male germ cells.