Abstract
KS58, one out of six known alleles of the small optic lobes (sol) gene in Drosophila melanogaster, reduces the cell number in the medulla cortex by degeneration of ganglion cells in the pupae to about 50%. Also, about half the volume of the medulla and lobula complex neuropils is missing. Many Golgistained cells in the mutant optic lobes resemble their homologues in wild type. However, special classes of transmedullary columnar neurons projecting to the lobula or to both lobula and lobula plate are not seen in the mutant. Some neurons linking the lobula complex to the central brain send branches to the medulla (the branches do not exist in wild type); some other types seem to be missing. The fate mapping of the KS58 focus reveals a location ventral to the head bristles and in sine oculis (so) flies the mutation further reduces the rudiments of the optic lobes normally seen. Therefore the sol phenotype is not induced by mutant eyes and the primary gene action seems to be on nervous tissue. The structural alterations of the small optic lobes are reflected in visual orientation behavior. The optomotor yaw response, however, is almost quantitatively preserved. The respective neural network should still be present in the mutant optic lobes.
Keywords: cell degeneration, developmental plasticity, orientation behavior, Golgi staining, genetic mosaics
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