ocr-2
C. elegans
Ion transport domain-containing protein
What the model saw
Gene: ocr-2 Organism: Caenorhabditis elegans Known functions: Ion transport domain-containing protein. calcium channel activity. monoatomic ion channel activity. temperature-gated cation channel activity.
View unredacted entry
Ion transport domain-containing protein. calcium channel activity. monoatomic ion channel activity. temperature-gated cation channel activity.
Solver output
OCR-2 is a TRPV (transient receptor potential vanilloid) channel in C. elegans that mediates calcium influx in sensory neurons, particularly in ASH and other chemosensory neurons. Calcium signaling through OCR-2 modulates neuroendocrine communication, including the release of neuropeptides that regulate systemic physiology and stress responses. Loss-of-function mutations in ocr-2 have been shown to extend lifespan in C. elegans, likely by reducing sensory perception of food/environmental cues and dampening insulin/IGF-1-like signaling (IIS) from sensory neurons, similar to other sensory neuron mutants. The temperature-gated cation channel activity places it in thermosensory circuits that influence DAF-16/FOXO-dependent longevity pathways. Thus, the normal (wild-type) function of ocr-2 promotes sensory signaling that activates pro-aging IIS, making its normal function anti-longevity; however, given the complexity of sensory neuron calcium signaling in both promoting and opposing stress responses, the predominant evidence points to wild-type ocr-2 activity shortening lifespan.
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's reasoning correctly identifies the mechanism (OCR-2 as a TRPV channel in sensory neurons that promotes IIS signaling, making wild-type function anti-longevity), and even explicitly states "the normal (wild-type) function of ocr-2 promotes sensory signaling that activates pro-aging IIS, making its normal function anti-longevity." However, the model's final prediction label is "pro_longevity" — the opposite of the ground truth "anti_longevity." This is a contradiction within the model's own reasoning: the reasoning concludes anti-longevity but the prediction field says pro_longevity. This appears to be a labeling confusion — the model may have confused "loss-of-function extends lifespan" (meaning wild-type is anti-longevity) with the pro_longevity label. The mechanism described is largely correct, but the final answer is wrong.
Raw API responses
solver
{
"reasoning": "OCR-2 is a TRPV (transient receptor potential vanilloid) channel in C. elegans that mediates calcium influx in sensory neurons, particularly in ASH and other chemosensory neurons. Calcium signaling through OCR-2 modulates neuroendocrine communication, including the release of neuropeptides that regulate systemic physiology and stress responses. Loss-of-function mutations in ocr-2 have been shown to extend lifespan in C. elegans, likely by reducing sensory perception of food/environmental cues and dampening insulin/IGF-1-like signaling (IIS) from sensory neurons, similar to other sensory neuron mutants. The temperature-gated cation channel activity places it in thermosensory circuits that influence DAF-16/FOXO-dependent longevity pathways. Thus, the normal (wild-type) function of ocr-2 promotes sensory signaling that activates pro-aging IIS, making its normal function anti-longevity; however, given the complexity of sensory neuron calcium signaling in both promoting and opposing stress responses, the predominant evidence points to wild-type ocr-2 activity shortening lifespan.",
"confidence": 0.55,
"key_pathways": [
"insulin/IGF-1 signaling (IIS) via sensory neuron neuroendocrine output",
"TRPV calcium channel-mediated sensory transduction",
"DAF-16/FOXO transcription factor regulation"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's reasoning correctly identifies the mechanism (OCR-2 as a TRPV channel in sensory neurons that promotes IIS signaling, making wild-type function anti-longevity), and even explicitly states \"the normal (wild-type) function of ocr-2 promotes sensory signaling that activates pro-aging IIS, making its normal function anti-longevity.\" However, the model's final prediction label is \"pro_longevity\" — the opposite of the ground truth \"anti_longevity.\" This is a contradiction within the model's own reasoning: the reasoning concludes anti-longevity but the prediction field says pro_longevity. This appears to be a labeling confusion — the model may have confused \"loss-of-function extends lifespan\" (meaning wild-type is anti-longevity) with the pro_longevity label. The mechanism described is largely correct, but the final answer is wrong.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}