AI Article Synopsis
- The study focuses on how the Wnt-secretory factor MIG-14/Wntless helps C. elegans neurons avoid overlapping dendrites, which is critical for neural function.
- Findings show that mutations in mig-14 lead to dendrite overlap, while increasing MIG-14 levels causes dendrites to push apart, highlighting its role in self-avoidance.
- Additionally, the research reveals that MIG-14's involvement in dendrite self-avoidance is separate from its role in Wnt secretion and involves a mechanism that relies on actin assembly.
Article Abstract
Self-avoidance allows sister dendrites from the same neuron to form non-redundant coverage of the sensory territory and is important for neural circuitry functions. Here, we report an unexpected, cell-autonomous role of the Wnt-secretory factor MIG-14/Wntless in mediating dendrite self-avoidance in the C. elegans multidendritic PVD neurons. Similar findings in Drosophila suggest that this novel function of Wntless is conserved. The mig-14 mutant shows defects in dendrite self-avoidance, and ectopic MIG-14 expression triggers dendrite repulsion. Functions of dendrite self-avoidance and Wnt secretion could be mapped to distinct MIG-14 domains, indicating that these two functions of MIG-14 are genetically separable, consistent with lack of self-avoidance defects in the Wnt mutants. We further demonstrate that MIG-14 engages Wiskott-Aldrich syndrome protein (WASP)-dependent actin assembly to regulate dendrite self-avoidance. Our work expands the repertoire of self-avoidance molecules and uncovers a previously unknown, Wnt-independent function of MIG-14/Wntless.
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| http://dx.doi.org/10.1016/j.neuron.2018.03.031 | DOI Listing |
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