The transmembrane LRR protein DMA-1 promotes dendrite branching and growth in C. elegans

Dendrites often adopt complex branched structures. The development and organization of these arbors fundamentally determine the potential input and connectivity of a given neuron. The cell-surface receptors that control dendritic branching remain poorly understood. We found that, in Caenorhabditis elegans, a previously uncharacterized transmembrane protein containing extracellular leucine-rich repeat (LRR) domains, which we named DMA-1 (dendrite-morphogenesis-abnormal), promotes dendrite branching and growth. Sustained expression of dma-1 was found only in the elaborately branched sensory neurons PVD and FLP. Genetic analysis revealed that the loss of dma-1 resulted in much reduced dendritic arbors, whereas overexpression of dma-1 resulted in excessive branching. Forced expression of dma-1 in neurons with simple dendrites was sufficient to promote ectopic branching. Worms lacking dma-1 were defective in sensing harsh touch. DMA-1 is the first transmembrane LRR protein to be implicated in dendritic branching and expands the breadth of roles of LRR receptors in nervous system development.