Most mitotic mutants in Drosophila do not lead to lethality in early development despite the highly abnormal chromosome behaviour that they elicit. This has been explained as being the effect of maternally provided wild-type products. We have tested this hypothesis by studying cuticular clones derived from cells in which there has been loss of a marked Y chromosome due to chromosome nondisjunction in individuals homozygous for the mutation abnormal spindle who are progeny of heterozygous mothers. We have found that the size and frequency of these clones are higher than in control flies. Furthermore, by analysing flies whose female parents have different doses of the asp+ gene, we have found that there is a correlation between the amount of maternally contributed asp+ product and the frequency and size of cuticular clones. We have also estimated the time in development when the first mitotic mistakes take place, i.e. the time when maternal products are no longer sufficient to carry out normal cell division.
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.
The wing blade of Drosophila melanogaster is composed of dorsal and ventral surfaces covered with hairs and rows of morphologically distinct bristles round the margin. The mutant shaggy causes a complete transformation of hairs into bristles over the entire wing surfaces. Clones of mutant bristles have a tendency to line up into straight bristle rows. Clones are straight and orderly near the wing margin but form bundles and vesicles when a long distance from the margin. Furthermore the bristle cells move distally along the future wing blade in the general direction of the margin. From these studies, we postulate the existence of a gradient of cell affinities for bristle cells that is maximal at the dorsoventral wing margin and decreases with distance away from it. The bristle clones also move onto the wing veins and often induce the formation of new veins in the surrounding shaggy+ cells. These new veins run from the clone and join up to existing veins. We conclude that there is a close relationship between bristles and veins.
Clones of cells mutant for shaggy transform all hairs into bristles on the wing blade of Drosophila. Different types of bristles are formed at different locations. It is shown that, although shaggy cells are unable to make a correct decision between an epidermal cell pathway and that of a sensory bristle, they are nevertheless able to respond correctly to positional cues. A compilation of many clones led to the construction of a map of positional homologies in which all of the cells in any one area will produce the same kind of bristle. The result is a series of stripes oriented perpendicular to the anteroposterior axis of the wing and parallel to the dorsoventral axis. The significance of these stripes in relation to mechanisms of pattern formation is discussed.