"Like humans, mice with an intact CALHM1 gene avidly drink sucrose and other sweeteners, and avoid bitter compounds such as quinine. However, mice lacking CALHM1 are very unusual," said Tordoff. "These mice treat sweeteners and bitter compounds as if they were water. They behave as if they can't taste them at all."
Responses to salty and sour tastes were not affected by the missing gene because perception of these taste qualities is mediated via a different set of taste cells.
In combination with electrophysiological data contributed by collaborators from other institutions, the findings demonstrate that pannexins and connexins, channel proteins previously thought to be involved in ATP release from taste cells, actually are not necessary for this to happen. "This paper provides compelling data to overturn the previous hypothesis," noted Matsumato. "It's part of what makes science so exciting."
Kevin Foskett, PhD, professor of Physiology at the Perelman School of Medicine, University of Pennsylvania, who with Marambaud is a senior author on the paper, recently identified CALHM1 as an ATP channel and speculated that that it might be involved in taste. "This is an example of a bona fide ATP ion channel with a clear physiological function," said Foskett. "Now we can connect the molecular dots of sweet and other tastes to the brain."
In addition to revealing CALHM1's critical role in sweet, bitter, and umami taste perception, the current work also lends insight into the channel's overall function in other tissues. Originally thought to control calcium levels inside cells, CALHM1 (calcium-homeostasis-modulator-1) may also contribute to ATP-mediated intercellular communication in the brain and elsewhere.
|Contact: Leslie Stein|
Monell Chemical Senses Center