Since spermatogenesis in Drosophila is a series of interconnected and interdependent steps and most of the spermatogenic events take place in the absence of transcription, failures in a given stage can give rise to a cascade of defects later on. The asp locus of Drosophila melanogaster codes for a non-tubulin component implicated in proper spindle structure and/or function (Ripoll et al. 1985). Homozygous asp males exhibit abnormal meiotic spindles giving rise to altered segregation of chromosomes and mitochondria and failures in cytokinesis. Postmeiotic spermatogenic stages of asp males show a series of alterations that we interpret as due to the previously occurring defective meiosis because meiotic spindles are the only microtubular structure altered in mutant testes. The most conspicuous alterations are: (i) variable size of nuclei and nebenkerns of early spermatids, which are also multinucleate instead of having single and uniformly sized nuclei; (ii) elongating spermatids in which abnormal-sized mitochondrial derivatives elongate alongside more than one axoneme; (iii) failures in the individualization process, where abnormal spermatids remain syncytial, and seem to be eliminated during the coiling stage.

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