Spermatogenesis inDrosophila hydei: A genetic survey

Abstract

We constructed balancer-chromosomes for the large autosomes ofDrosophila hydei and screened more than 16000 chromosomes for male sterile mutations in order to dissect spermatogenesis genetically. 365 mutants on the X chromosome and the autosomes 2, 3, and 4 were recovered and analysed cytologically in squash preparations under phase-contrast optics. The majority of the mutations allows a rather advanced differentiation of the spermatozoa. At the light-microscopical level, it is possible to classify these mutations with respect to individualization, coiling or motility of the mutant spermatozoa. In contrast, a small number of mutants exhibits conspicuous, pleiotropic phenotypes. Gonial divisions, the shaping of the spermatocyte nucleus and male meiotic divisions are controlled by X chromosomal or autosomal genes which can mutate to male sterile alleles. A number of nonallelic 3 chromosome male sterile mutations interfere with the unfolding of the Y chromosomal lampbrush loops. Other autosomal male sterile mutations modify the morphology of these lampbrush loops. Another group of mutations inhibits the formation of the nebenkern while the development of the spermatid nucleus and the flagellum can proceed. Such male sterile mutations can decouple the development of nucleus, protein body, nebenkern, and flagellum of the spermatid. Thus, we can describe spermatogenesis inDrosophila as the coordinate execution of the individual developmental programs of the different components of the spermatozoon.

The Comparative Genetics of Human Spermatogenesis: Clues from Flies and Other Model Organisms

“…Equal diameters of nuclei are indicative of a correct chromosome segregation, and the formation of equally sized nebenkerne (which result from a fusion of all mitochrondria of a spermatid) IS indicative of normal cytokinesis (cf. Hackstein et al 1990). …”

“…The answer is that most genes are. The phenotypic analysis of the male sterile mutants reveals that only a few male sterile mutants might lack progeny due to morphological modifications of the testis, the genital tract or the copulation organs (Lindsley and Tokuyasu 1980;Hackstein et al 1990;Castrillon et al 1993). There is also little evidence that behavioural abnormalities are a frequent cause of infertility, because, with a few exceptions, sterile male flies that are capable of producing motile spermatozoa, are also able to transfer sperm cells to females.…”

“…However, mutations with a paternal lethal effect are extremely rare. The vast majority (about 80%) of the Drosophila mutants produce elongated, but immotile sperm that degenerate prior to individualization -regardless of the method of mutagenization (Hackstein et al 1990;Hackstein 1991;Castrillon et al 1993). Using an electron microscope, disorganized flagella and abnormal mitochondrial derivatives are seen (Fuller 1993).…”

“…The screening of 16000 X chromosomes and autosomes 2,3 and 4 yielded 365 male sterile mutants (Hackstein et al 1990). All mutants were analyzed for testis morphology, cytology, sperm differentiation and their ability to transfer sperm to the receptaculum seminis of female flies (Hackstein 1991).…”

“…All stages of male germ cell differentiation are found in a single testis. After gentle squashing, the different stages can be examined under a light microscope using phase contrast optics, with well-defined cytogenetic landmarks for many stages (Lindsley and Tokuyasu 1980;Hennig 1985;Hackstein et al 1990;Fuller 1993;Cenci et al 1994). For instance, the normal completion of meiosis can be followed by counting the number of spermatid nuclei and mitochondrial derivatives per cyst.…”