Sister dendrites from the same neuron show self-avoidance, a conserved mechanism among different nervous system to pattern non-overlapping dendritic arborization. Cell surface proteins, such as Dscam and protocadherins, and secreted cues, including Netrin and Slit, are known to regulate dendrite self-avoidance. Here we show that the Wnt-secretory factor MIG-14/Wntless controlled dendrite self-avoidance in the C. elegans multidendritic PVD neurons. This unexpected function of MIG-14 was independent of Wnts, as none of the Wnt or Wnt receptor mutants examined showed PVD self-avoidance defects, and MIG-14 acted cell-autonomously in the PVD, rather than in the Wnt-secreting tissues, to regulate self-avoidance. MIG-14 function was required during the establishment of PVD dendrite self-avoidance. Movements of MIG-14 molecules in the PVD dendrites required UNC-116/Kinesin 1, and mutation in unc-116 caused self-avoidance defects. MIG-14 showed homophilic interaction when expressed in mammalian cells. Our structure-function analysis suggested that the first extracellular domain was required for dendrite self-avoidance, whereas the C-terminus domain was dispensable. Ectopic MIG-14 expression triggered defasciculation of tightly bundled nerve ring branches of the touch neurons. We propose that MIG-14 mediates dendrite self-avoidance through contact-dependent repulsion. Our findings expand the repertoire of self-avoidance factors and uncover a previously unknown, Wnt-independent function of MIG-14/Wntless. (supported by the Ministry of Science and Technology, Taiwan, 103-2320-B-002-050-MY3).
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