Send to

Choose Destination
Nat Neurosci. 2011 Dec 4;15(1):57-63. doi: 10.1038/nn.2978.

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

Author information

Howard Hughes Medical Institute, Department of Biology, Stanford University, Stanford, California, USA.


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center