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inf-1

C. elegans

Eukaryotic initiation factor 4A

What the model saw

Gene: inf-1
Organism: Caenorhabditis elegans
Known functions: Eukaryotic initiation factor 4A. ATP binding. ATP hydrolysis activity. RNA helicase activity. nucleic acid binding. translation initiation factor activity.
View unredacted entry
Eukaryotic initiation factor 4A. ATP binding. ATP hydrolysis activity. RNA helicase activity. nucleic acid binding. translation initiation factor activity.

Solver output

Predicted influence
Anti-longevity
Confidence
75%
Mechanism
Deregulated nutrient sensing
Reasoning

inf-1 encodes the C. elegans eukaryotic initiation factor 4A (eIF4A), an ATP-dependent RNA helicase that unwinds secondary structures in the 5' UTR of mRNAs to facilitate ribosome recruitment during cap-dependent translation initiation. eIF4A is a core component of the eIF4F complex, which is a major downstream effector of the mTORC1/TOR nutrient-sensing pathway. In C. elegans, reduced global translation — achieved by downregulating components of the translation initiation machinery including eIF4A — is a well-established pro-longevity intervention; loss-of-function of translation initiation factors extends lifespan. Therefore, the normal (wild-type) activity of inf-1 promotes robust cap-dependent translation, which opposes longevity by sustaining high mTOR-driven protein synthesis rates and suppressing the translational attenuation that extends lifespan.

Key pathways
mTORC1/TOR signaling - cap-dependent translation initiationeIF4F complex assembly and RNA helicase activityglobal protein synthesis regulation
Longevity influence
Unclear
Lifespan effect
Increase and Decrease

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

Answer
Incorrect
Mechanism
Incorrect
Reasoning quality
3/5
Failure mode
Confident wrong
Notes

The ground truth is "unclear" but the model predicted "anti_longevity" with 0.75 confidence. The model's reasoning is plausible in general terms — eIF4A/translation initiation factors are indeed linked to TOR signaling and reduced translation can extend lifespan in C. elegans — but the actual evidence for inf-1 specifically is apparently insufficient to make a clear determination, hence "unclear" in GenAge. The model was overconfident (0.75) in assigning a definitive anti-longevity role when the evidence is ambiguous. The mechanistic reasoning is coherent but not specifically supported by experimental data on inf-1 in C. elegans longevity, making it speculative extrapolation rather than evidence-based classification.

Raw API responses

solver

{
  "reasoning": "inf-1 encodes the C. elegans eukaryotic initiation factor 4A (eIF4A), an ATP-dependent RNA helicase that unwinds secondary structures in the 5' UTR of mRNAs to facilitate ribosome recruitment during cap-dependent translation initiation. eIF4A is a core component of the eIF4F complex, which is a major downstream effector of the mTORC1/TOR nutrient-sensing pathway. In C. elegans, reduced global translation — achieved by downregulating components of the translation initiation machinery including eIF4A — is a well-established pro-longevity intervention; loss-of-function of translation initiation factors extends lifespan. Therefore, the normal (wild-type) activity of inf-1 promotes robust cap-dependent translation, which opposes longevity by sustaining high mTOR-driven protein synthesis rates and suppressing the translational attenuation that extends lifespan.",
  "confidence": 0.75,
  "key_pathways": [
    "mTORC1/TOR signaling - cap-dependent translation initiation",
    "eIF4F complex assembly and RNA helicase activity",
    "global protein synthesis regulation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The ground truth is \"unclear\" but the model predicted \"anti_longevity\" with 0.75 confidence. The model's reasoning is plausible in general terms — eIF4A/translation initiation factors are indeed linked to TOR signaling and reduced translation can extend lifespan in C. elegans — but the actual evidence for inf-1 specifically is apparently insufficient to make a clear determination, hence \"unclear\" in GenAge. The model was overconfident (0.75) in assigning a definitive anti-longevity role when the evidence is ambiguous. The mechanistic reasoning is coherent but not specifically supported by experimental data on inf-1 in C. elegans longevity, making it speculative extrapolation rather than evidence-based classification.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}