The Drosophila peripheral nervous system comprises four major types of sensory element: external sense organs (such as mechano-sensory bristles), chordotonal organs (internal stretch receptors), multiple dendritic neurons, and photoreceptors. During development, the selection of neural precursors for external sense organs requires the proneural genes of the achaete-scute complex, which encode basic-helix-loop-helix transcription factors. These genes do not, however, control precursor selection for chordotonal organs or photoreceptors, raising the question of whether other proneural genes exist or a different mechanism of neurogenesis operates. Here we show that atonal (ato), originally isolated as a proneural gene for chordotonal organs, is also the proneural gene for photoreceptors. Pattern formation in the Drosophila eye involves a succession of cell fate specifications. Of the eight photoreceptors within each ommatidium of the compound eye, the photoreceptor R8 is the first to appear in the eye imaginal disc, right behind the morphogenetic furrow. The appearance of other photoreceptors (R1-7) follows in a defined sequence that is thought to arise by induction from R8 (refs 8, 9, 11, 12). We find that photoreceptor formation requires the function of atonal at the morphogenetic furrow and that atonal is specifically required for R8 selection. Formation of other photoreceptors does not directly require atonal function, but does depend on R8 selection by atonal. Thus, photoreceptors are selected by two mechanisms: R8 by a proneural mechanism, and R1-7 by local recruitment.

A P-element vector has been constructed and used to generate lines of flies with single autosomal P-element insertions. The lines were analyzed in two ways: (1) the identification of cis-acting patterning information within the Drosophila genome, as revealed by a lacZ reporter gene within the P element, and (2) the isolation of lethal mutations. We examined 3768 independent lines for the expression of lacZ in embryos and looked among these lines for lethal mutations affecting embryonic neurogenesis. This type of screen appears to be an effective way to find new loci that may play a role in the development of the Drosophila nervous system.[Key Words: P element; lacZ; mutagenesis; cell market; Drosophila; pattern]Received May 30, 1989; revised version accepted July 11, 1989. One approach to studying development is to obtain genetic variants that are defective in some crucial step. This type of genetic analysis has been very successful in identifying virtually all of the zygotic loci required for the early stages of segmentation during embryogenesis in Drosophila melanogaster Niisslein-Volhard et al. 1984;Wieschaus et al. 1984). Besides chemical mutagenesis, transposon tagging has been used as a mutagen and allows rapid cloning of genes of interest (Bingham et al. 1981;Kidwell 1986).Recently, a scheme wherein single P elements are mobilized to new chromosomal locations has been implemented successfully (Cooley et al. 1988). The essential nature of this approach is to use two separate P elements to provide the two functions necessary for transposition. The first is a genetically marked P element that is defective in production of transposase but contains the ends required for its own transposition. The second is a P element with functional transposase activity but a much reduced likelihood for its own transposition (Robertson et al. 1988). Transposition of the marked P element then is initiated by crossing flies that carry only the marked P element to those that harbor only transposase. Insertions generated by this scheme are recovered in flies lacking tranposase activity and are therefore genetically stable.P-element vectors also have been used recently to search for cis-acting sequences which confer tissue-specific expression of a p-galactosidase [lacZ] fusion gene driven by the weak promoter of the P-element transpoPresent addresses:

Neurons contain distinct compartments including dendrites, dendritic spines, axons and synaptic terminals. The molecular mechanisms that generate and distinguish these compartments, although largely unknown, may involve the small GTPases Rac and Cdc42, which appear to regulate actin polymerization. Having shown that perturbations of Rac1 activity block the growth of axons but not dendrites of Drosophila neurons, we investigated whether this also applies to mammals by examining transgenic mice expressing constitutively active human Rac1 in Purkinje cells. We found that these mice were ataxic and had a reduction of Purkinje-cell axon terminals in the deep cerebellar nuclei, whereas the dendritic trees grew to normal height and branched extensively. Unexpectedly, the dendritic spines of Purkinje cells in developing and mature cerebella were much reduced in size but increased in number. These 'mini' spines often form supernumerary synapses. These differential effects of perturbing Rac1 activity indicate that there may be distinct mechanisms for the elaboration of axons, dendrites and dendritic spines.

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