Evidence for Two Populations of Bitter Responsive Taste Cells in Mice

Hacker, Kyle; Laskowski, Agnes; Feng, Linyin; Restrepo, Diego; Medler, Kathryn F.

doi:10.1152/jn.00892.2007

Cited by 48 publications

(67 citation statements)

References 43 publications

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“…For the taste samples collected from P0 mice, the epithelium was peeled and the CV was closely cropped to minimize the amount of non-taste tissue included. Isolated taste receptor cells were harvested from the adult CV papillae as previously described (Hacker et al, 2008) for qPCR, western blot and ChIP experiments.…”

Section: Taste Cell Isolationmentioning

confidence: 99%

WT1 regulates the development of the posterior taste field

et al. 2014

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Despite the importance of taste in determining nutrient intake, our understanding of the processes that control the development of the peripheral taste system is lacking. Several early regulators of taste development have been identified, including sonic hedgehog, bone morphogenetic protein 4 and multiple members of the Wnt/β-catenin signaling pathway. However, the regulation of these factors, including their induction, remains poorly understood. Here, we identify a crucial role for the Wilms' tumor 1 protein (WT1) in circumvallate (CV) papillae development. WT1 is a transcription factor that is important in the normal development of multiple tissues, including both the olfactory and visual systems. In mice, WT1 expression is detectable by E12.5, when the CV taste placode begins to form. In mice lacking WT1, the CV fails to develop normally and markers of early taste development are dysregulated compared with wild type. We demonstrate that expression of the WT1 target genes Lef1, Ptch1 and Bmp4 is significantly reduced in developing tongue tissue derived from Wt1 knockout mice and that, in normal tongue, WT1 is bound to the promoter regions of these genes. Moreover, siRNA knockdown of WT1 in cultured taste cells leads to a reduction in the expression of Lef1 and Ptch1. Our data identify WT1 as a crucial transcription factor in the development of the CV through the regulation of multiple signaling pathways that have established roles in the formation and patterning of taste placodes.

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Section: Taste Cell Isolationmentioning

confidence: 99%

WT1 regulates the development of the posterior taste field

et al. 2014

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“…Isolated taste receptor cells were loaded for 40 min with 2 M fura 2-AM (Invitrogen, Carlsbad, CA) containing the nonionic dispersing agent Pluronic F-127 (Invitrogen) as previously described (Hacker et al 2008). Loaded cells were visualized using an Olympus IX71 microscope with a 40ϫ oil immersion lens, and images were captured using a Sensicam QE camera (Cooke, Romulus, MI).…”

Section: Calcium Imagingmentioning

confidence: 99%

“…Taste receptor cells were easily identified by their characteristic morphology (Hacker et al 2008). The calcium signaling mechanisms expressed by taste cells were identified using two different stimuli.…”

Section: Identification Of Taste Cells and Their Calcium Signaling Pamentioning

confidence: 99%

“…Dependence on calcium release was determined by the cell's responsiveness to a 20-s application of a bitter mixture (see Solutions). We have previously shown that responsiveness to these two types of stimuli are caused by calcium influx for VGCCs and calcium release from internal stores for the bitter mixture (Hacker et al 2008). Since we are discussing these taste cells in terms of how they handle their calcium loads, i.e., taste cells that have a very large calcium load because of calcium influx through VGCCs versus taste cells that rely on calcium release from internal stores in response to taste stimuli, we will refer to these taste cells as taste cells with calcium release or with calcium influx/VGCC.…”

Section: Identification Of Taste Cells and Their Calcium Signaling Pamentioning

confidence: 99%

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Mitochondrial Calcium Buffering Contributes to the Maintenance of Basal Calcium Levels in Mouse Taste Cells

Hacker¹,

Medler²

2008

Journal of Neurophysiology

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Hacker K, Medler KF. Mitochondrial calcium buffering contributes to the maintenance of basal calcium levels in mouse taste cells. J Neurophysiol 100: 2177-2191. First published August 6, 2008 doi:10.1152/jn.90534.2008. Taste stimuli are detected by taste receptor cells present in the oral cavity using diverse signaling pathways. Some taste stimuli are detected by G protein-coupled receptors (GPCRs) that cause calcium release from intracellular stores, whereas other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). Although taste cells use two distinct mechanisms to transmit taste signals, increases in cytosolic calcium are critical for normal responses in both pathways. This creates a need to tightly control intracellular calcium levels in all transducing taste cells. To date, however, the mechanisms used by taste cells to regulate cytosolic calcium levels have not been identified. Studies in other cell types have shown that mitochondria can be important calcium buffers, even during small changes in calcium loads. In this study, we used calcium imaging to characterize the role of mitochondria in buffering calcium levels in taste cells. We discovered that mitochondria make important contributions to the maintenance of resting calcium levels in taste cells by routinely buffering a constitutive calcium influx across the plasma membrane. This is unusual because in other cell types, mitochondrial calcium buffering primarily affects large evoked calcium responses. We also found that the amount of calcium that is buffered by mitochondria varies with the signaling pathways used by the taste cells. A transient receptor potential (TRP) channel, likely TRPV1 or a taste variant of TRPV1, contributes to the constitutive calcium influx. I N T R O D U C T I O NThe detection of gustatory stimuli depends on the activation of taste receptor cells located in taste buds within the oral cavity. Activated taste receptors on the apical membrane of taste cells initiate transduction pathways that ultimately transmit signals to afferent gustatory neurons. Taste cells use two distinct signaling pathways to mediate their communication to the nervous system: 1) calcium influx through voltage-gated calcium channels (VGCCs), which causes vesicular neurotransmitter release or 2) G proteincoupled receptor (GPCR)-dependent second messenger pathways that activate a calcium-dependent nonvesicular mechanism to release the neurotransmitter, ATP (Clapp et al. 2004(Clapp et al. , 2006DeFazio et al. 2006;Finger et al. 2005;Huang et al. 2007;Romanov et al. 2007;Tomchik et al. 2007). Both signaling mechanisms depend on increasing cytosolic calcium to produce normal synaptic signals. Hence all transducing taste cells must tightly regulate intracellular calcium levels. Currently, the role of buffering mechanisms to control cytosolic calcium levels in taste cells has not been described.In addition to its role in ATP production, mitochondria make significant contributions to the regulation cytosolic calci...

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“…This chemical prevents the taste cells of rats (Rössler et al, 1998), mudpuppies (Ogura & Kinnamon, 1999 and mice (Sawano et al, 2005;Hacker et al, 2008) from perceiving denatonium. Effective concentrations of U-73122 ranged from 1 μM to 10 μM.…”

Section: Effects Of Signal Transduction Modulators On Feeding Commencmentioning

confidence: 99%

Pharmacological analysis of the feeding response of codling moth (Cydia pomonella; Lepidoptera: Tortricidae) neonates to bitter compounds

Pszczółkowski¹

2017

Eur. J. Entomol.

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Abstract. Feeding in codling moth neonate caterpillars was inhibited by 0.67 mM and 2.24 mM concentrations of denatonium benzoate. This inhibitory effect was abolished by phospholipase C inhibitor, U-73122 and the phosphodiesterase inhibitor, Rolipram. Quinine and quinidine did not have inhibitory effects at concentrations as high as 1.64 mM and 0.43 mM, respectively. The inhibitory effect of denatonium was partially reversed in the presence of the calcium ion chelator, EGTA, at concentrations ranging from 2.5 μM to 250 μM. These results indicate that transduction of the taste of denatonium in codling moth neonates relies on signalling pathways that involve phospholipase C, phosphodiesterase and calcium ion infl ux into cells.

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Evidence for Two Populations of Bitter Responsive Taste Cells in Mice

Abstract: Evidence for two populations of bitter responsive taste cells in mice.

Cited by 48 publications

References 43 publications

WT1 regulates the development of the posterior taste field

WT1 regulates the development of the posterior taste field

Mitochondrial Calcium Buffering Contributes to the Maintenance of Basal Calcium Levels in Mouse Taste Cells

Pharmacological analysis of the feeding response of codling moth (Cydia pomonella; Lepidoptera: Tortricidae) neonates to bitter compounds

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