We have used a retrograde labeling technique to identify motorneurons for each of the 30 body wall muscles of an abdominal hemisegment in the late stage 16 Drosophila embryo. Each motorneuron has a characteristic cell body position, dendritic arborization, and axonal projection. In addition, we have determined the neuroblasts of origin for most of the motorneurons we describe. Some organizational principles for the neuromuscular system have become apparent: (1) There is no obvious topographic relationship between the cell body positions of motorneurons and the position or orientation of the muscles they innervate; (2) motorneurons that innervate muscles of similar position and orientation are often clustered and have overlapping dendritic trees; (3) morphologically similar motorneurons are generally derived from a common neuroblast and innervate operationally related muscles; and (4) neuroblasts can give rise to more than one morphological type of motorneuron.

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Cell-shape changes during development require a precise coupling of the cytoskeleton with proteins situated in the plasma membrane. Important elements controlling the shape of cells are the Spectrin proteins that are expressed as a subcortical cytoskeletal meshwork linking specific membrane receptors with F-actin fibers. Here, we demonstrate that Drosophila karussell mutations affect ␤-spectrin and lead to distinct axonal patterning defects in the embryonic CNS. karussell mutants display a slitsensitive axonal phenotype characterized by axonal looping in stage-13 embryos. Further analyses of individual, labeled neuroblast lineages revealed abnormally structured growth cones in these animals. Cell-type-specific rescue experiments demonstrate that ␤-Spectrin is required autonomously and non-autonomously in cortical neurons to allow normal axonal patterning. Within the cell, ␤-Spectrin is associated with ␣-Spectrin. We show that expression of the two genes is tightly regulated by post-translational mechanisms. Loss of ␤-Spectrin significantly reduces levels of neuronal ␣-Spectrin expression, whereas gain of ␤-Spectrin leads to an increase in ␣-Spectrin protein expression. Because the loss of ␣-spectrin does not result in an embryonic nervous system phenotype, ␤-Spectrin appears to act at least partially independent of ␣-Spectrin to control axonal patterning.

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