期刊
NEURON
卷 98, 期 3, 页码 547-+出版社
CELL PRESS
DOI: 10.1016/j.neuron.2018.03.043
关键词
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资金
- NIH [R01DC012538, R37GM048071, R01AG053988, R01DC015491, R01EY015537, R03DC014328]
- JSPS KAKENHI [26713008, 16K15181, 25670111, 15K15034]
- Salt Science [1542]
- Society for Research on Umami Taste
- Grants-in-Aid for Scientific Research [16K15181, 26713008, 15K15034, 25670111] Funding Source: KAKEN
Binding of sweet, umami, and bitter tastants to G protein-coupled receptors (GPCRs) in apical membranes of type II taste bud cells (TBCs) triggers action potentials that activate a voltage-gated nonselective ion channel to release ATP to gustatory nerves mediating taste perception. Although calcium homeostasis modulator 1 (CALHM1) is necessary for ATP release, the molecular identification of the channel complex that provides the conductive ATP-release mechanism suitable for action potential-dependent neurotransmission remains to be determined. Here we show that CALHM3 interacts with CALHM1 as a pore-forming subunit in a CALHM1/CALHM3 hexameric channel, endowing it with fast voltage-activated gating identical to that of the ATP-release channel in vivo. Calhm3 is co-expressed with Calhm1 exclusively in type II TBCs, and its genetic deletion abolishes taste-evoked ATP release from taste buds and GPCR-mediated taste perception. Thus, CALHM3, together with CALHM1, is essential to form the fast voltage-gated ATP-release channel in type II TBCs required for GPCR-mediated tastes.
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