Abstract

COVER PHOTOGRAPH: Drosophila embryonic axons visualized for expression of Fasciclin II (red) and a transgene that marks sema‐phorin2b‐positive cells (green). semaphorin2b‐positive axons deviate from their normal Fasciclin II tracts in both the lateral and ventral direction in semaphorin2b mutants (upper right) compared to wildtype (upper left). From Drosophila semaphorin2b is Required for the Axon Guidance of a Subset of Embryonic Neurons, Mark M. Emerson, Jennifer B. Long, and David Van Vactor, Developmental Dynamics 242:861–873, 2013.

Highlights

  • A key component in the development of the nervous system is the process of axon guidance in which a neuron extends a process to its post-synaptic target

  • While the immense complexity of some nervous systems suggested that many signaling pathways are employed during development, it has become increasingly clear that several conserved pathways are used repeatedly to shape the development of different neural circuits throughout the embryo

  • We adopted a misexpression approach in the Drosophila embryo to aid in the recovery of differentially expressed factors that contribute to the specificity of individual axon guidance decisions

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Summary

Background

The process of axon guidance is important in establishing functional neural circuits. Results: We report the characterization of a predicted secreted semaphorin family member, semaphorin2b (Sema-2b) in Drosophila embryonic axon guidance. Misexpression of Sema-2b in neurons causes highly penetrant axon guidance phenotypes in specific longitudinal and motoneuron pathways; expression of Sema-2b in muscles traversed by these motoneurons has no effect on axon guidance. Conclusions: While secreted semaphorins have been implicated as cell non-autonomous chemorepellants in a variety of contexts, here we report previously undescribed Sema-2b loss-of-function and misexpression phenotypes that are consistent with a cell-autonomous role for Sema-2b. VC 2013 Wiley Periodicals, Inc. Key Findings: Misexpression of the secreted semaphorin Sema-2b in neurons results in specific axon guidance phenotypes. Key Findings: Misexpression of the secreted semaphorin Sema-2b in neurons results in specific axon guidance phenotypes Both Sema-2b loss-of-function and misexpression phenotypes are congruent with a cell-autonomous role for Sema-2b. Novel axon guidance phenotypes caused by Sema-2b loss-of-function mutations are characterized

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