Abstract
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 β-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 β-Spectrin is required autonomously and non-autonomously in cortical neurons to allow normal axonal patterning. Within the cell, β-Spectrin is associated with α-Spectrin. We show that expression of the two genes is tightly regulated by post-translational mechanisms. Loss of β-Spectrin significantly reduces levels of neuronal α-Spectrin expression, whereas gain of β-Spectrin leads to an increase in α-Spectrin protein expression. Because the loss of α-spectrin does not result in an embryonic nervous system phenotype, β-Spectrin appears to act at least partially independent of α-Spectrin to control axonal patterning.
Original language | English (US) |
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Pages (from-to) | 713-722 |
Number of pages | 10 |
Journal | Development |
Volume | 134 |
Issue number | 4 |
DOIs | |
State | Published - Feb 2007 |
Externally published | Yes |
Keywords
- Drosophila
- Growth cone
- Nervous system
- Spectrin
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology