ife-1
C. elegans
Eukaryotic translation initiation factor 4E-1;eIF-4F 25 kDa subunit
What the model saw
Gene: ife-1 Organism: Caenorhabditis elegans Known functions: Eukaryotic translation initiation factor 4E-1;eIF-4F 25 kDa subunit. RNA 7-methylguanosine cap binding. RNA binding. RNA trimethylguanosine cap binding. protein binding. translation initiation factor activity.
View unredacted entry
Eukaryotic translation initiation factor 4E-1;eIF-4F 25 kDa subunit. RNA 7-methylguanosine cap binding. RNA binding. RNA trimethylguanosine cap binding. protein binding. translation initiation factor activity.
Solver output
ife-1 encodes one of five eIF4E paralogs in C. elegans, functioning as the cap-binding subunit of the eIF4F translation initiation complex. Reduced global translation is a well-established pro-longevity mechanism in C. elegans (e.g., knockdown of ife-2 extends lifespan), operating downstream of nutrient-sensing pathways such as TOR/TORC1, which phosphorylates 4E-BP to release eIF4E and promote cap-dependent translation. However, ife-1 is a specific paralog with preferential expression in the germline and distinct substrate specificity compared to ife-2 or ife-3; its loss does not consistently extend lifespan in the same manner as ife-2 knockdown. Because the longevity effect of eIF4E paralogs in C. elegans is highly paralog-specific, and ife-1's primary role appears germline-restricted rather than somatic, the net influence on organismal longevity is genuinely ambiguous without additional context.
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 predicted "unclear" while the ground truth is "anti_longevity" (meaning ife-1 promotes longevity when lost, i.e., its normal function shortens lifespan). The model correctly identified that ife-1 is a germline-expressed eIF4E paralog and that different paralogs have different longevity effects, but it failed to commit to the correct answer. The model's reasoning about paralog-specificity is sound but incomplete - it knew ife-2 knockdown extends lifespan but didn't extend this logic to conclude ife-1 is likely also anti-longevity. The mechanism class of "deregulated_nutrient_sensing" is partially relevant (TOR pathway connection) but not the most precise framing. The model's uncertainty was somewhat reasonable given the paralog complexity, but the ground truth indicates ife-1 is clearly anti-longevity, suggesting the model should have leaned more toward that conclusion given the general principle that translation initiation factors tend to be anti-longevity in C. elegans.
Raw API responses
solver
{
"reasoning": "ife-1 encodes one of five eIF4E paralogs in C. elegans, functioning as the cap-binding subunit of the eIF4F translation initiation complex. Reduced global translation is a well-established pro-longevity mechanism in C. elegans (e.g., knockdown of ife-2 extends lifespan), operating downstream of nutrient-sensing pathways such as TOR/TORC1, which phosphorylates 4E-BP to release eIF4E and promote cap-dependent translation. However, ife-1 is a specific paralog with preferential expression in the germline and distinct substrate specificity compared to ife-2 or ife-3; its loss does not consistently extend lifespan in the same manner as ife-2 knockdown. Because the longevity effect of eIF4E paralogs in C. elegans is highly paralog-specific, and ife-1's primary role appears germline-restricted rather than somatic, the net influence on organismal longevity is genuinely ambiguous without additional context.",
"confidence": 0.45,
"key_pathways": [
"eIF4F cap-dependent translation initiation",
"TOR/TORC1 nutrient sensing",
"germline translation regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity\" (meaning ife-1 promotes longevity when lost, i.e., its normal function shortens lifespan). The model correctly identified that ife-1 is a germline-expressed eIF4E paralog and that different paralogs have different longevity effects, but it failed to commit to the correct answer. The model's reasoning about paralog-specificity is sound but incomplete - it knew ife-2 knockdown extends lifespan but didn't extend this logic to conclude ife-1 is likely also anti-longevity. The mechanism class of \"deregulated_nutrient_sensing\" is partially relevant (TOR pathway connection) but not the most precise framing. The model's uncertainty was somewhat reasonable given the paralog complexity, but the ground truth indicates ife-1 is clearly anti-longevity, suggesting the model should have leaned more toward that conclusion given the general principle that translation initiation factors tend to be anti-longevity in C. elegans.",
"failure_mode": "appropriately_uncertain",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}