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First published online 10 January 2007
doi: 10.1242/dev.02758

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Distinct functions of -Spectrin and ß-Spectrin during axonal pathfinding

Jörn Hülsmeier¹, Jan Pielage^1,*, Christof Rickert², Gerd M. Technau², Christian Klämbt^1, and Tobias Stork¹

¹ Institut für Neurobiologie, Badestr. 9, 48149 Münster, Germany.
² Institut für Genetik, Saarstr. 21, 64123 Mainz, Germany.

Author for correspondence (e-mail: klaembt{at}uni-muenster.de)

Accepted 27 November 2006

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 ß-spectrin and lead to distinct axonal patterning defects in the embryonic CNS. karussell mutants display a slit-sensitive 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 ß-Spectrin is required autonomously and non-autonomously in cortical neurons to allow normal axonal patterning. Within the cell, ß-Spectrin is associated with -Spectrin. We show that expression of the two genes is tightly regulated by post-translational mechanisms. Loss of ß-Spectrin significantly reduces levels of neuronal -Spectrin expression, whereas gain of ß-Spectrin leads to an increase in -Spectrin protein expression. Because the loss of -spectrin does not result in an embryonic nervous system phenotype, ß-Spectrin appears to act at least partially independent of -Spectrin to control axonal patterning.

Key words: Spectrin, Drosophila, Growth cone, Nervous system

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