Sarco/Endoplasmic Reticulum Ca2+-ATPases (SERCA) Contribute to GPCR-Mediated Taste Perception
Open Access
- 2 August 2011
- journal article
- research article
- Published by Public Library of Science (PLoS) in PLOS ONE
- Vol. 6 (8), e23165
- https://doi.org/10.1371/journal.pone.0023165
Abstract
The sense of taste is important for providing animals with valuable information about the qualities of food, such as nutritional or harmful nature. Mammals, including humans, can recognize at least five primary taste qualities: sweet, umami (savory), bitter, sour, and salty. Recent studies have identified molecules and mechanisms underlying the initial steps of tastant-triggered molecular events in taste bud cells, particularly the requirement of increased cytosolic free Ca2+ concentration ([Ca2+]c) for normal taste signal transduction and transmission. Little, however, is known about the mechanisms controlling the removal of elevated [Ca2+]c from the cytosol of taste receptor cells (TRCs) and how the disruption of these mechanisms affects taste perception. To investigate the molecular mechanism of Ca2+ clearance in TRCs, we sought the molecules involved in [Ca2+]c regulation using a single-taste-cell transcriptome approach. We found that Serca3, a member of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) family that sequesters cytosolic Ca2+ into endoplasmic reticulum, is exclusively expressed in sweet/umami/bitter TRCs, which rely on intracellular Ca2+ release for signaling. Serca3-knockout (KO) mice displayed significantly increased aversive behavioral responses and greater gustatory nerve responses to bitter taste substances but not to sweet or umami taste substances. Further studies showed that Serca2 was mainly expressed in the T1R3-expressing sweet and umami TRCs, suggesting that the loss of function of Serca3 was possibly compensated by Serca2 in these TRCs in the mutant mice. Our data demonstrate that the SERCA family members play an important role in the Ca2+ clearance in TRCs and that mutation of these proteins may alter bitter and perhaps sweet and umami taste perception.This publication has 62 references indexed in Scilit:
- Calcium Signaling in Taste Cells: Regulation RequiredChemical Senses, 2010
- The cells and peripheral representation of sodium taste in miceNature, 2010
- The Candidate Sour Taste Receptor, PKD2L1, Is Expressed by Type III Taste Cells in the MouseChemical Senses, 2007
- The role of pannexin 1 hemichannels in ATP release and cell–cell communication in mouse taste budsProceedings of the National Academy of Sciences of the United States of America, 2007
- Afferent neurotransmission mediated by hemichannels in mammalian taste cellsThe EMBO Journal, 2007
- The cells and logic for mammalian sour taste detectionNature, 2006
- Transient receptor potential family members PKD1L3 and PKD2L1 form a candidate sour taste receptorProceedings of the National Academy of Sciences of the United States of America, 2006
- Nucleoside triphosphate diphosphohydrolase‐2 is the ecto‐ATPase of type I cells in taste budsJournal of Comparative Neurology, 2006
- Coding of Sweet, Bitter, and Umami Tastes: Different Receptor Cells Sharing Similar Signaling PathwaysCell, 2003
- A transient receptor potential channel expressed in taste receptor cellsNature Neuroscience, 2002