Abstract
Repulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance. Here we report the function of the Caenorhabditis elegans ortholog DRAG-1 in axon branching. The axons of hermaphrodite-specific neurons (HSNs) extend dorsal branches at the region abutting the vulval muscles. The drag-1 mutants exhibited defects in HSN axon branching in addition to a small body size phenotype. DRAG-1 expression in the hypodermal cells was required for the branching of the axons. Although DRAG-1 is normally expressed in the ventral hypodermis excepting the vulval region, its ectopic expression in vulval precursor cells was sufficient to induce the branching. The C-terminal glycosylphosphatidylinositol anchor of DRAG-1 was important for its function, suggesting that DRAG-1 should be anchored to the cell surface. Genetic analyses suggested that the membrane receptor UNC-40 acts in the same pathway with DRAG-1 in HSN branching. We propose that DRAG-1 expressed in the ventral hypodermis signals via the UNC-40 receptor expressed in HSNs to elicit branching activity of HSN axons.
Highlights
Repulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance
We examined the morphology of the axon of hermaphrodite specific neurons (HSNs) using kyIs262[unc86p::myrGFP; odr-1::RFP]20 as a transgenic marker
We have shown that the sole C. elegans repulsive guidance molecule DRAG-1 functions in hypodermal cells to regulate axon branching of the hermaphrodite-specific neurons (HSNs) that form synapses with the vulval egg-laying muscles in hermaphrodites
Summary
Repulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance. Ephrins are membrane-bound molecules that abolish branching of thalamic a xons[3] In addition to these well-known guidance molecules, repulsive guidance molecules (RGMs) repress axon branching in cortical neurons and mossy fibers of the h ippocampus[4,5]. By binding to the membrane receptor neogenin, RGMs function in axon guidance and neuronal survival as well as inhibition of axonal regeneration[8,9,10]. We showed that drag-1 expressed in the hypodermis functions in the formation of branches of hermaphrodite-specific neurons (HSNs), which innervate egg-laying muscles of the v ulva[17]. Small body size mutants sma-1 and sma-5 exhibited HSN axon branching defects they act in genetic pathways distinct from that of drag-1
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