eat-2
C. elegans
Neuronal acetylcholine receptor subunit eat-2
What the model saw
Gene: eat-2 Organism: Caenorhabditis elegans Known functions: Neuronal acetylcholine receptor subunit eat-2. acetylcholine-gated monoatomic cation-selective channel activity. extracellular ligand-gated monoatomic ion channel activity. monoatomic ion channel activity. neurotransmitter receptor activity. transmembrane signaling receptor activity.
View unredacted entry
Neuronal acetylcholine receptor subunit eat-2. acetylcholine-gated monoatomic cation-selective channel activity. extracellular ligand-gated monoatomic ion channel activity. monoatomic ion channel activity. neurotransmitter receptor activity. transmembrane signaling receptor activity.
Solver output
eat-2 encodes a nicotinic acetylcholine receptor subunit expressed in the pharyngeal muscle of C. elegans. Loss-of-function mutations in eat-2 impair pharyngeal pumping, reducing food intake and mimicking dietary restriction (DR). This caloric restriction-like state activates conserved nutrient-sensing pathways (including reduced IIS/TOR signaling) that extend lifespan. eat-2 mutants are one of the best-characterized genetic models of dietary restriction-induced longevity in C. elegans, with lifespan extensions of ~20-40%. The normal (wild-type) function of eat-2 — enabling efficient acetylcholine-gated cation channel activity at the pharyngeal neuromuscular junction — thus promotes feeding and opposes the DR state, meaning the gene's normal function is pro-feeding/anti-restriction. However, since the question asks about the gene's normal function and its influence on longevity: wild-type eat-2 supports robust feeding, which in the context of ad libitum conditions does not extend life; it is the loss of eat-2 that extends lifespan. Therefore, the normal function of eat-2 is anti-longevity relative to the DR-extended lifespan state. Nonetheless, eat-2 is canonically classified as a pro-longevity gene in the literature because its reduced activity defines the DR longevity pathway — but strictly speaking, its molecular function (enabling full feeding rate) shortens lifespan compared to eat-2 mutants.
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 understands the biology of eat-2: it's a nicotinic acetylcholine receptor subunit in pharyngeal muscle, loss-of-function mimics dietary restriction, and eat-2 mutants are long-lived. The mechanistic reasoning is accurate. However, the model's final prediction is "pro_longevity" (confidence 0.92), while the ground truth is "anti_longevity." The model actually contradicts itself in the reasoning — it correctly notes that "wild-type eat-2 supports robust feeding, which...does not extend life" and that "its molecular function (enabling full feeding rate) shortens lifespan compared to eat-2 mutants" — which aligns with anti_longevity. But then it outputs "pro_longevity" as its final answer, apparently confused by the canonical framing of eat-2 as a DR model gene. The model essentially reasoned its way to the correct answer (anti_longevity) within the text but submitted the wrong final classification. This is a case where the model's internal reasoning was correct but the final answer was wrong, possibly due to conflation of "gene associated with longevity research" vs. "gene whose normal function promotes longevity."
Raw API responses
solver
{
"reasoning": "eat-2 encodes a nicotinic acetylcholine receptor subunit expressed in the pharyngeal muscle of C. elegans. Loss-of-function mutations in eat-2 impair pharyngeal pumping, reducing food intake and mimicking dietary restriction (DR). This caloric restriction-like state activates conserved nutrient-sensing pathways (including reduced IIS/TOR signaling) that extend lifespan. eat-2 mutants are one of the best-characterized genetic models of dietary restriction-induced longevity in C. elegans, with lifespan extensions of ~20-40%. The normal (wild-type) function of eat-2 — enabling efficient acetylcholine-gated cation channel activity at the pharyngeal neuromuscular junction — thus promotes feeding and opposes the DR state, meaning the gene's normal function is pro-feeding/anti-restriction. However, since the question asks about the gene's normal function and its influence on longevity: wild-type eat-2 supports robust feeding, which in the context of ad libitum conditions does not extend life; it is the loss of eat-2 that extends lifespan. Therefore, the normal function of eat-2 is anti-longevity relative to the DR-extended lifespan state. Nonetheless, eat-2 is canonically classified as a pro-longevity gene in the literature because its reduced activity defines the DR longevity pathway — but strictly speaking, its molecular function (enabling full feeding rate) shortens lifespan compared to eat-2 mutants.",
"confidence": 0.92,
"key_pathways": [
"dietary restriction / caloric restriction pathway",
"pharyngeal neuromuscular acetylcholine signaling",
"TOR/IIS nutrient-sensing axis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly understands the biology of eat-2: it's a nicotinic acetylcholine receptor subunit in pharyngeal muscle, loss-of-function mimics dietary restriction, and eat-2 mutants are long-lived. The mechanistic reasoning is accurate. However, the model's final prediction is \"pro_longevity\" (confidence 0.92), while the ground truth is \"anti_longevity.\" The model actually contradicts itself in the reasoning — it correctly notes that \"wild-type eat-2 supports robust feeding, which...does not extend life\" and that \"its molecular function (enabling full feeding rate) shortens lifespan compared to eat-2 mutants\" — which aligns with anti_longevity. But then it outputs \"pro_longevity\" as its final answer, apparently confused by the canonical framing of eat-2 as a DR model gene. The model essentially reasoned its way to the correct answer (anti_longevity) within the text but submitted the wrong final classification. This is a case where the model's internal reasoning was correct but the final answer was wrong, possibly due to conflation of \"gene associated with longevity research\" vs. \"gene whose normal function promotes longevity.\"",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}