title: The transmembrane LRR protein DMA-1 promotes dendrite branching and growth in C. elegans.
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. 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.
authors.affiliation: Howard Hughes Medical Institute, Department of Biology, Stanford University, Stanford, California, USA.
authors.forename: Oliver W
authors.initials: OW
authors.lastname: Liu
authors.forename: Kang
authors.initials: K
authors.lastname: Shen
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D017173:Caenorhabditis elegans; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism*; D003712:Dendrites / Q000235:genetics / Q000378:metabolism*; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*
chemical_list: D029742:Caenorhabditis elegans Proteins; C569907:DMA-1 protein, C elegans; D008565:Membrane Proteins