Premium
Drosophila semaphorin2b is required for the axon guidance of a subset of embryonic neurons
Author(s) -
Emerson Mark M.,
Long Jennifer B.,
Van Vactor David
Publication year - 2013
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.23979
Subject(s) - semaphorin , axon guidance , biology , axon , neuroscience , phenotype , embryonic stem cell , growth cone , cell type , plexin , microbiology and biotechnology , cell , genetics , gene , receptor
Background: The process of axon guidance is important in establishing functional neural circuits. The differential expression of cell‐autonomous axon guidance factors is crucial for allowing axons of different neurons to take unique trajectories in response to spatially and temporally restricted cell non‐autonomous axon guidance factors. A key motivation in the field is to provide adequate explanations for axon behavior with respect to the differential expression of these factors. 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; however, expression of Sema‐2b in muscles traversed by these motoneurons has no effect on axon guidance. In Sema‐2b loss‐of‐function embryos, specific motoneuron and interneuron axon pathways display guidance defects. Specific visualization of the neurons that normally express Sema‐2b reveals that this neuronal cohort is strongly affected by Sema‐2b loss‐of‐function alleles. 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 . Developmental Dynamics 242:861–873, 2013 . © 2013 Wiley Periodicals, Inc.