Question:hard
Sour taste is mediated by:
Sour taste is mediated by:
Show Hint
Sweet/umami/bitter use T1R/T2R GPCRs; salty uses ENaC; sour senses \(H^+\) via a proton channel (OTOP1). Match the option to the paper key.
Updated On: Jun 22, 2026
- TRPV3 Channel
- Metabolic receptors
- GPCR T1R1
- GPCR T1Ra
Show Solution
The Correct Option is D
Solution and Explanation
Tackle this by sorting each taste modality by its molecular sensor, then placing the printed options.
The map of taste transduction:
- Sweet = GPCR heterodimer T1R2 + T1R3.
- Umami = GPCR heterodimer T1R1 + T1R3.
- Bitter = GPCR family T2R.
- Salty = ENaC epithelial sodium channel.
- Sour = sensing of protons (\[H^+\]) by type III taste cells, chiefly through the OTOP1 (otopetrin-1) proton channel, with PKD2L1 historically associated.
Apply to the choices: TRPV3 is a temperature-sensitive TRP channel of skin/keratinocytes, not a taste-quality receptor. 'Metabolic receptors' is not a recognised sour-taste sensor. T1R1 is specifically the umami partner receptor, so option C belongs to umami, not sour. That leaves the generic GPCR taste-receptor option (D), which the examiner accepted as the key for this recalled question.
Mechanism of sour transduction in detail: Acidic foods raise extracellular \[H^+\]; protons enter type III taste receptor cells largely through the OTOP1 proton channel, acidifying the cytoplasm. This intracellular acidification blocks resting \[K^+\] channels and depolarises the cell, triggering action potentials and neurotransmitter (serotonin) release onto the gustatory afferent fibres. This is a fundamentally different signalling route from the second-messenger cascades (gustducin, PLCβ, \[IP_3\], TRPM5) used downstream of the sweet/bitter/umami GPCRs.
Important caveat: In current physiology, sour taste is an ion-channel (proton/OTOP1) mechanism rather than a true GPCR mechanism; if an OTOP1 / proton-channel choice were available it would be the most accurate. Given only these four options, the paper's marked answer is D.
$Answer = D$ (as per the official key); concept-wise, sour is best explained by the $OTOP1$ proton channel.
The map of taste transduction:
- Sweet = GPCR heterodimer T1R2 + T1R3.
- Umami = GPCR heterodimer T1R1 + T1R3.
- Bitter = GPCR family T2R.
- Salty = ENaC epithelial sodium channel.
- Sour = sensing of protons (\[H^+\]) by type III taste cells, chiefly through the OTOP1 (otopetrin-1) proton channel, with PKD2L1 historically associated.
Apply to the choices: TRPV3 is a temperature-sensitive TRP channel of skin/keratinocytes, not a taste-quality receptor. 'Metabolic receptors' is not a recognised sour-taste sensor. T1R1 is specifically the umami partner receptor, so option C belongs to umami, not sour. That leaves the generic GPCR taste-receptor option (D), which the examiner accepted as the key for this recalled question.
Mechanism of sour transduction in detail: Acidic foods raise extracellular \[H^+\]; protons enter type III taste receptor cells largely through the OTOP1 proton channel, acidifying the cytoplasm. This intracellular acidification blocks resting \[K^+\] channels and depolarises the cell, triggering action potentials and neurotransmitter (serotonin) release onto the gustatory afferent fibres. This is a fundamentally different signalling route from the second-messenger cascades (gustducin, PLCβ, \[IP_3\], TRPM5) used downstream of the sweet/bitter/umami GPCRs.
Important caveat: In current physiology, sour taste is an ion-channel (proton/OTOP1) mechanism rather than a true GPCR mechanism; if an OTOP1 / proton-channel choice were available it would be the most accurate. Given only these four options, the paper's marked answer is D.
$Answer = D$ (as per the official key); concept-wise, sour is best explained by the $OTOP1$ proton channel.
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