Journal
GENES TO CELLS
Volume 17, Issue 9, Pages 778-789Publisher
WILEY
DOI: 10.1111/j.1365-2443.2012.01627.x
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Funding
- NIH National Center for Research Resources
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan
- Japan Society for the Promotion of Science (JSPS)
- Japan Science and Technology Agency (JST)
- Grants-in-Aid for Scientific Research [23229001, 24390053, 24657081, 23370083] Funding Source: KAKEN
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Ras-family GTPases regulate a wide variety of cellular functions including cell growth and differentiation. Di-Ras, which belongs to a distinct subfamily of Ras-family GTPases, is expressed predominantly in brain, but the role of Di-Ras in nervous systems remains totally unknown. Here, we report that the Caenorhabditis elegans Di-Ras homologue drn-1 is expressed specifically in neuronal cells and involved in synaptic function at neuromuscular junctions. Loss of function of drn-1 conferred resistance to the acetylcholinesterase inhibitor aldicarb and partially suppressed the aldicarb-hypersensitive phenotypes of heterotrimeric G-protein mutants, in which acetylcholine release is up-regulated. drn-1 mutants displayed no apparent defects in the axonal distribution of the membrane-bound second messenger diacylglycerol (DAG), which is a key stimulator of acetylcholine release. Finally, we have identified EPAC-1, a C.similar to elegans Epac homologue, as a binding partner for DRN-1. Deletion mutants of epac-1 displayed an aldicarb-resistant phenotype as drn-1 mutants. Genetic analysis of drn-1 and epac-1 showed that they acted in the same pathway to control acetylcholine release. Furthermore, DRN-1 and EPAC-1 were co-immunoprecipitated. These findings suggest that DRN-1 may function cooperatively with EPAC-1 to modulate synaptic activity in C.similar to elegans.
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