Abstract
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. Here, we show that in Caenorhabditis elegans, a previously uncharacterized transmembrane protein containing extracellular leucine-rich repeat (LRR) domains, which we name DMA-1 (Dendrite-Morphogenesis-Abnormal), promotes dendrite branching and growth. Sustained expression of dma-1 is found only in the elaborately branched sensory neurons PVD and FLP. Genetic analysis showed that loss of dma-1 causes much reduced dendritic arbors while overexpression of dma-1 results in excessive branching. Forced expression of dma-1 in neurons with simple dendrites was sufficient to promote ectopic branching. Animals lacking dma-1 are 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 played by LRR receptors in nervous system development.
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