trpa-1
C. elegans
Ion transport domain-containing protein;Transient receptor potential cation channel subfamily A member 1 homolog
What the model saw
Gene: trpa-1 Organism: Caenorhabditis elegans Known functions: Ion transport domain-containing protein;Transient receptor potential cation channel subfamily A member 1 homolog. monoatomic ion channel activity.
View unredacted entry
Ion transport domain-containing protein;Transient receptor potential cation channel subfamily A member 1 homolog. monoatomic ion channel activity.
Solver output
TRPA-1 is the C. elegans homolog of the TRPA1 transient receptor potential cation channel, which mediates ion flux (particularly Ca²⁺ and Na⁺) across cellular membranes in response to noxious stimuli and reactive electrophiles. In C. elegans, trpa-1 has been shown to function in sensory neurons to detect oxidative and electrophilic stress signals, coupling environmental sensing to downstream longevity pathways. TRP channel-mediated calcium signaling in sensory neurons can modulate neuroendocrine communication, influencing systemic stress responses and lifespan. Specifically, TRPA-1 activity has been linked to activation of the DAF-16/FOXO transcription factor pathway, a central pro-longevity axis in C. elegans, through calcium-dependent signaling cascades. Loss of trpa-1 has been reported to shorten lifespan, consistent with a pro-longevity role for the channel's normal function in coordinating stress-responsive intercellular signaling.
GenAge curators classify each gene's normal function as promoting (Pro-Longevity) or opposing (Anti-Longevity) longevity, based on synthesis across studies. Loss-of-function effects can vary from this depending on the manipulation.
Advisor judgment
The model correctly predicted pro_longevity for trpa-1 in C. elegans with reasonable confidence (0.62). The mechanistic reasoning is well-grounded: TRPA-1 functions as a TRP channel in sensory neurons, mediates calcium signaling in response to oxidative/electrophilic stress, and connects to DAF-16/FOXO pathway. The claim that loss of trpa-1 shortens lifespan is consistent with published literature (Kindt et al. and related work). The mechanism class of "altered_intercellular_communication" is reasonable given the neuroendocrine signaling aspect, though one could argue stress response signaling is equally valid. Overall a solid, well-reasoned prediction.
Raw API responses
solver
{
"reasoning": "TRPA-1 is the C. elegans homolog of the TRPA1 transient receptor potential cation channel, which mediates ion flux (particularly Ca²⁺ and Na⁺) across cellular membranes in response to noxious stimuli and reactive electrophiles. In C. elegans, trpa-1 has been shown to function in sensory neurons to detect oxidative and electrophilic stress signals, coupling environmental sensing to downstream longevity pathways. TRP channel-mediated calcium signaling in sensory neurons can modulate neuroendocrine communication, influencing systemic stress responses and lifespan. Specifically, TRPA-1 activity has been linked to activation of the DAF-16/FOXO transcription factor pathway, a central pro-longevity axis in C. elegans, through calcium-dependent signaling cascades. Loss of trpa-1 has been reported to shorten lifespan, consistent with a pro-longevity role for the channel's normal function in coordinating stress-responsive intercellular signaling.",
"confidence": 0.62,
"key_pathways": [
"TRP channel-mediated calcium signaling",
"DAF-16/FOXO transcription factor pathway",
"neuroendocrine stress response communication"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for trpa-1 in C. elegans with reasonable confidence (0.62). The mechanistic reasoning is well-grounded: TRPA-1 functions as a TRP channel in sensory neurons, mediates calcium signaling in response to oxidative/electrophilic stress, and connects to DAF-16/FOXO pathway. The claim that loss of trpa-1 shortens lifespan is consistent with published literature (Kindt et al. and related work). The mechanism class of \"altered_intercellular_communication\" is reasonable given the neuroendocrine signaling aspect, though one could argue stress response signaling is equally valid. Overall a solid, well-reasoned prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}