eif-3.K
C. elegans
Eukaryotic translation initiation factor 3 subunit K
What the model saw
Gene: eif-3.K Organism: Caenorhabditis elegans Known functions: Eukaryotic translation initiation factor 3 subunit K. RNA binding. ribosome binding. translation initiation factor activity.
View unredacted entry
Eukaryotic translation initiation factor 3 subunit K. RNA binding. ribosome binding. translation initiation factor activity.
Solver output
eif-3.K encodes subunit K of the eukaryotic translation initiation factor 3 (eIF3) complex, which is a core regulator of cap-dependent translation initiation. In C. elegans, global translation rate is tightly coupled to nutrient-sensing pathways, particularly TOR (mTORC1) signaling, which phosphorylates downstream effectors to promote ribosome recruitment and translation. Partial loss-of-function of eIF3 subunits reduces overall translational output, mimicking the effects of TOR inhibition or dietary restriction, both of which are well-established pro-longevity interventions in C. elegans. Reduced translation initiation via eIF3 subunit knockdown has been shown to extend lifespan in worms, consistent with the broader principle that attenuating protein synthesis rates reduces proteotoxic stress and energy expenditure. The RNA-binding and ribosome-binding activities of eif-3.K place it directly at the mTOR–translation axis, where its normal (full) activity supports high translation rates that are associated with shorter lifespan; thus, its normal function is anti-longevity, but RNAi/reduction of this gene is pro-longevity. Since the question asks about the gene's normal function, full eIF3 activity promotes translation and 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 - it correctly identifies that eif-3.K promotes translation (anti-longevity function), and that reducing its activity extends lifespan. However, the model contradicts itself in the final answer. The reasoning concludes "full eIF3 activity promotes translation and opposes longevity" (i.e., anti-longevity), but then outputs "pro_longevity" as the longevity_influence. This is a self-contradictory answer where the reasoning leads to the correct conclusion (anti_longevity) but the final prediction is wrong (pro_longevity). The model seems confused about whether the question asks about the gene's effect when active (anti-longevity) vs. when knocked down (pro-longevity). The ground truth is anti_longevity, which matches the model's own reasoning but not its final answer.
Raw API responses
solver
{
"reasoning": "eif-3.K encodes subunit K of the eukaryotic translation initiation factor 3 (eIF3) complex, which is a core regulator of cap-dependent translation initiation. In C. elegans, global translation rate is tightly coupled to nutrient-sensing pathways, particularly TOR (mTORC1) signaling, which phosphorylates downstream effectors to promote ribosome recruitment and translation. Partial loss-of-function of eIF3 subunits reduces overall translational output, mimicking the effects of TOR inhibition or dietary restriction, both of which are well-established pro-longevity interventions in C. elegans. Reduced translation initiation via eIF3 subunit knockdown has been shown to extend lifespan in worms, consistent with the broader principle that attenuating protein synthesis rates reduces proteotoxic stress and energy expenditure. The RNA-binding and ribosome-binding activities of eif-3.K place it directly at the mTOR–translation axis, where its normal (full) activity supports high translation rates that are associated with shorter lifespan; thus, its normal function is anti-longevity, but RNAi/reduction of this gene is pro-longevity. Since the question asks about the gene's normal function, full eIF3 activity promotes translation and opposes longevity.",
"confidence": 0.62,
"key_pathways": [
"mTOR-translation initiation axis",
"cap-dependent translation (eIF3 complex)",
"dietary restriction / translational attenuation longevity pathway"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's mechanistic reasoning is actually correct - it correctly identifies that eif-3.K promotes translation (anti-longevity function), and that reducing its activity extends lifespan. However, the model contradicts itself in the final answer. The reasoning concludes \"full eIF3 activity promotes translation and opposes longevity\" (i.e., anti-longevity), but then outputs \"pro_longevity\" as the longevity_influence. This is a self-contradictory answer where the reasoning leads to the correct conclusion (anti_longevity) but the final prediction is wrong (pro_longevity). The model seems confused about whether the question asks about the gene's effect when active (anti-longevity) vs. when knocked down (pro-longevity). The ground truth is anti_longevity, which matches the model's own reasoning but not its final answer.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}