eef-2
C. elegans
Elongation factor 2
What the model saw
Gene: eef-2 Organism: Caenorhabditis elegans Known functions: Elongation factor 2. GTP binding. GTPase activity. ribosome binding. translation elongation factor activity.
View unredacted entry
Elongation factor 2. GTP binding. GTPase activity. ribosome binding. translation elongation factor activity.
Solver output
EEF-2 (Elongation Factor 2) is a GTPase that catalyzes the translocation step of ribosomal peptide-chain elongation, a rate-limiting step in global protein synthesis. In C. elegans, reduced translation elongation — achieved by partial loss-of-function of eef-2 — has been shown to extend lifespan, consistent with the broader paradigm that dampening mTORC1-driven translational output promotes longevity. The mTOR/nutrient-sensing pathway directly phosphorylates and inactivates EF2 kinase (which in turn inhibits EEF-2), so EEF-2 activity is a downstream effector of nutrient-sensing signaling. Reducing EEF-2 activity mimics dietary restriction at the translational level, decreasing the energetic burden of protein synthesis and activating stress-response pathways. Thus, the normal (full) function of eef-2 — promoting maximal translation elongation — is anti-longevity, while its reduction is pro-longevity; however, since the question asks about the gene's normal function, high EEF-2 activity opposes longevity by sustaining high translational rates downstream of nutrient-sensing pathways.
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 ground truth labels eef-2's longevity influence as "unclear," but the model confidently predicts "pro_longevity" with 0.78 confidence. The model's reasoning is internally contradictory — it first says reduced eef-2 extends lifespan (which would make it anti-longevity in normal function), then concludes the gene is "pro_longevity," which doesn't align with its own mechanistic argument. The model seems to conflate the effect of reducing the gene (which may extend lifespan) with the gene itself being "pro_longevity." If anything, the model's own reasoning would suggest the gene is anti-longevity (since its normal function opposes longevity). The mechanism around mTOR/EF2 kinase/EEF-2 is plausible but oversimplified and the final classification contradicts the reasoning. The ground truth "unclear" designation suggests the evidence is ambiguous, which the model fails to acknowledge despite its contradictory reasoning being a signal of that ambiguity.
Raw API responses
solver
{
"reasoning": "EEF-2 (Elongation Factor 2) is a GTPase that catalyzes the translocation step of ribosomal peptide-chain elongation, a rate-limiting step in global protein synthesis. In C. elegans, reduced translation elongation — achieved by partial loss-of-function of eef-2 — has been shown to extend lifespan, consistent with the broader paradigm that dampening mTORC1-driven translational output promotes longevity. The mTOR/nutrient-sensing pathway directly phosphorylates and inactivates EF2 kinase (which in turn inhibits EEF-2), so EEF-2 activity is a downstream effector of nutrient-sensing signaling. Reducing EEF-2 activity mimics dietary restriction at the translational level, decreasing the energetic burden of protein synthesis and activating stress-response pathways. Thus, the normal (full) function of eef-2 — promoting maximal translation elongation — is anti-longevity, while its reduction is pro-longevity; however, since the question asks about the gene's normal function, high EEF-2 activity opposes longevity by sustaining high translational rates downstream of nutrient-sensing pathways.",
"confidence": 0.78,
"key_pathways": [
"mTOR/nutrient-sensing → translation elongation",
"ribosomal translocation (GTPase-driven peptide-chain elongation)",
"dietary restriction mimicry via reduced translational output"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The ground truth labels eef-2's longevity influence as \"unclear,\" but the model confidently predicts \"pro_longevity\" with 0.78 confidence. The model's reasoning is internally contradictory — it first says reduced eef-2 extends lifespan (which would make it anti-longevity in normal function), then concludes the gene is \"pro_longevity,\" which doesn't align with its own mechanistic argument. The model seems to conflate the effect of reducing the gene (which may extend lifespan) with the gene itself being \"pro_longevity.\" If anything, the model's own reasoning would suggest the gene is anti-longevity (since its normal function opposes longevity). The mechanism around mTOR/EF2 kinase/EEF-2 is plausible but oversimplified and the final classification contradicts the reasoning. The ground truth \"unclear\" designation suggests the evidence is ambiguous, which the model fails to acknowledge despite its contradictory reasoning being a signal of that ambiguity.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}