ifta-2
C. elegans
Intraflagellar transport associated protein 2
What the model saw
Gene: ifta-2 Organism: Caenorhabditis elegans Known functions: Intraflagellar transport associated protein 2. GTPase activity.
View unredacted entry
Intraflagellar transport associated protein 2. GTPase activity.
Solver output
ifta-2 encodes an intraflagellar transport (IFT)-associated GTPase in C. elegans. IFT proteins are essential for the assembly and maintenance of cilia, which in C. elegans sensory neurons (amphid neurons) serve as the primary sensory organelles that detect environmental signals including food/nutrient cues. Ciliary signaling in C. elegans modulates the DAF-2/insulin-IGF-1 pathway: ciliated sensory neurons release neuroendocrine signals (including insulin-like peptides) that activate DAF-2, suppressing DAF-16/FOXO and shortening lifespan. Loss-of-function mutations in IFT genes (e.g., osm-5, che-2) disrupt cilia and reduce insulin-like signaling, thereby de-repressing DAF-16 and extending lifespan. By analogy, ifta-2's GTPase activity supports IFT and cilia integrity; its normal function thus sustains pro-aging insulin/IGF-1 signaling from sensory neurons, meaning the gene itself is anti-longevity in its normal role. However, several IFT-associated proteins have been shown to promote longevity through non-canonical roles, introducing some uncertainty. The dominant interpretation from the IFT/cilia-DAF-2 axis places ifta-2 as pro-longevity when its loss extends lifespan, but the gene's normal function (maintaining cilia that drive DAF-2 signaling) is more accurately anti-longevity. Re-evaluating: the normal function of ifta-2 maintains cilia → maintains DAF-2 signaling → suppresses DAF-16 → shortens lifespan, making it anti-longevity.
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 final submitted answer is "pro_longevity," which is incorrect — the ground truth is "anti_longevity." However, the model's reasoning actually arrives at the correct mechanistic conclusion (ifta-2 maintains cilia → sustains DAF-2/insulin-IGF-1 signaling → suppresses DAF-16 → shortens lifespan → anti_longevity). The model explicitly re-evaluates and states "making it anti-longevity" at the end of its reasoning, yet still submits "pro_longevity" as its final answer. This is a clear contradiction between the reasoning and the submitted prediction. The mechanism described is largely correct, but the final answer field is wrong, making this a case of right reasoning but wrong answer submitted.
Raw API responses
solver
{
"reasoning": "ifta-2 encodes an intraflagellar transport (IFT)-associated GTPase in C. elegans. IFT proteins are essential for the assembly and maintenance of cilia, which in C. elegans sensory neurons (amphid neurons) serve as the primary sensory organelles that detect environmental signals including food/nutrient cues. Ciliary signaling in C. elegans modulates the DAF-2/insulin-IGF-1 pathway: ciliated sensory neurons release neuroendocrine signals (including insulin-like peptides) that activate DAF-2, suppressing DAF-16/FOXO and shortening lifespan. Loss-of-function mutations in IFT genes (e.g., osm-5, che-2) disrupt cilia and reduce insulin-like signaling, thereby de-repressing DAF-16 and extending lifespan. By analogy, ifta-2's GTPase activity supports IFT and cilia integrity; its normal function thus sustains pro-aging insulin/IGF-1 signaling from sensory neurons, meaning the gene itself is anti-longevity in its normal role. However, several IFT-associated proteins have been shown to promote longevity through non-canonical roles, introducing some uncertainty. The dominant interpretation from the IFT/cilia-DAF-2 axis places ifta-2 as pro-longevity when its loss extends lifespan, but the gene's normal function (maintaining cilia that drive DAF-2 signaling) is more accurately anti-longevity. Re-evaluating: the normal function of ifta-2 maintains cilia → maintains DAF-2 signaling → suppresses DAF-16 → shortens lifespan, making it anti-longevity.",
"confidence": 0.62,
"key_pathways": [
"Intraflagellar transport (IFT) / ciliogenesis",
"DAF-2/insulin-IGF-1 signaling",
"DAF-16/FOXO transcription factor regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's final submitted answer is \"pro_longevity,\" which is incorrect — the ground truth is \"anti_longevity.\" However, the model's reasoning actually arrives at the correct mechanistic conclusion (ifta-2 maintains cilia → sustains DAF-2/insulin-IGF-1 signaling → suppresses DAF-16 → shortens lifespan → anti_longevity). The model explicitly re-evaluates and states \"making it anti-longevity\" at the end of its reasoning, yet still submits \"pro_longevity\" as its final answer. This is a clear contradiction between the reasoning and the submitted prediction. The mechanism described is largely correct, but the final answer field is wrong, making this a case of right reasoning but wrong answer submitted.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}