osm-3
C. elegans
Osmotic avoidance abnormal protein 3
What the model saw
Gene: osm-3 Organism: Caenorhabditis elegans Known functions: Osmotic avoidance abnormal protein 3. ATP binding. ATP hydrolysis activity. microtubule binding. microtubule motor activity. plus-end-directed microtubule motor activity.
View unredacted entry
Osmotic avoidance abnormal protein 3. ATP binding. ATP hydrolysis activity. microtubule binding. microtubule motor activity. plus-end-directed microtubule motor activity.
Solver output
OSM-3 is a kinesin-2 family motor protein (KIF17 ortholog) that drives anterograde intraflagellar transport (IFT) along cilia in C. elegans sensory neurons. Its plus-end-directed microtubule motor activity, ATP hydrolysis, and microtubule binding are all hallmarks of IFT kinesin function. Proper IFT and ciliogenesis in amphid and phasmid sensory neurons is required for chemosensory and osmosensory signaling; loss of ciliary function in these neurons is well established to extend lifespan in C. elegans by reducing insulin/IGF-1-like signaling (IIS) through the DAF-2/DAF-16 axis. Specifically, ciliated sensory neurons produce neuroendocrine signals (including DAF-7/TGF-β and insulin-like peptides) that activate DAF-2 and suppress DAF-16/FOXO; when cilia are intact and functional, these pro-aging signals are efficiently transmitted, shortening lifespan. Thus, OSM-3's normal function maintains cilia integrity and thereby sustains pro-aging neuroendocrine output, making it pro-longevity when lost but anti-longevity in its normal active state. However, because osm-3 loss-of-function mutants live longer, the gene's normal function opposes 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 mechanistic reasoning is actually correct and well-articulated: OSM-3 maintains cilia integrity, which sustains pro-aging neuroendocrine signaling through the IIS/DAF-2/DAF-16 axis, meaning loss of OSM-3 extends lifespan. This correctly identifies OSM-3 as anti-longevity (its normal function opposes longevity). However, the model contradicts itself in its final answer - it explicitly states "osm-3 loss-of-function mutants live longer" and that "the gene's normal function opposes longevity," yet still outputs "pro_longevity" as the longevity_influence. The model's reasoning correctly identifies the gene as anti_longevity but then assigns the wrong label. This is a clear self-contradiction where the reasoning leads to the correct conclusion but the final answer is wrong. The ground truth is anti_longevity, and the model predicted pro_longevity despite its own reasoning pointing to anti_longevity.
Raw API responses
solver
{
"reasoning": "OSM-3 is a kinesin-2 family motor protein (KIF17 ortholog) that drives anterograde intraflagellar transport (IFT) along cilia in C. elegans sensory neurons. Its plus-end-directed microtubule motor activity, ATP hydrolysis, and microtubule binding are all hallmarks of IFT kinesin function. Proper IFT and ciliogenesis in amphid and phasmid sensory neurons is required for chemosensory and osmosensory signaling; loss of ciliary function in these neurons is well established to extend lifespan in C. elegans by reducing insulin/IGF-1-like signaling (IIS) through the DAF-2/DAF-16 axis. Specifically, ciliated sensory neurons produce neuroendocrine signals (including DAF-7/TGF-β and insulin-like peptides) that activate DAF-2 and suppress DAF-16/FOXO; when cilia are intact and functional, these pro-aging signals are efficiently transmitted, shortening lifespan. Thus, OSM-3's normal function maintains cilia integrity and thereby sustains pro-aging neuroendocrine output, making it pro-longevity when lost but anti-longevity in its normal active state. However, because osm-3 loss-of-function mutants live longer, the gene's normal function opposes longevity.",
"confidence": 0.72,
"key_pathways": [
"intraflagellar transport (IFT) / ciliogenesis",
"insulin/IGF-1 signaling (DAF-2/DAF-16 axis)",
"sensory neuron neuroendocrine signaling"
],
"mechanism_class": "other",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's mechanistic reasoning is actually correct and well-articulated: OSM-3 maintains cilia integrity, which sustains pro-aging neuroendocrine signaling through the IIS/DAF-2/DAF-16 axis, meaning loss of OSM-3 extends lifespan. This correctly identifies OSM-3 as anti-longevity (its normal function opposes longevity). However, the model contradicts itself in its final answer - it explicitly states \"osm-3 loss-of-function mutants live longer\" and that \"the gene's normal function opposes longevity,\" yet still outputs \"pro_longevity\" as the longevity_influence. The model's reasoning correctly identifies the gene as anti_longevity but then assigns the wrong label. This is a clear self-contradiction where the reasoning leads to the correct conclusion but the final answer is wrong. The ground truth is anti_longevity, and the model predicted pro_longevity despite its own reasoning pointing to anti_longevity.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}