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kra

D. melanogaster

krasavietz

What the model saw

Gene: kra
Organism: Drosophila melanogaster
Known functions: krasavietz. protein binding. ribosomal small subunit binding. ribosome binding. translation initiation factor binding.
View unredacted entry
krasavietz. protein binding. ribosomal small subunit binding. ribosome binding. translation initiation factor binding.

Solver output

Predicted influence
Pro-longevity
Confidence
62%
Mechanism
Loss of proteostasis
Reasoning

The krasavietz (kra) protein binds the ribosomal small subunit and translation initiation factors, placing it as a regulator of translational initiation. In the context of aging, reduced or fine-tuned translational output — particularly through modulation of ribosome activity and initiation factor interactions — is a well-established pro-longevity mechanism in model organisms including Drosophila. By binding and potentially inhibiting or modulating translation initiation factor activity at the small ribosomal subunit, kra may act as a translational brake, reducing global protein synthesis rates and thereby alleviating proteostatic stress. Reduced translation rates are linked to decreased mTORC1 signaling output and improved proteostasis, both of which extend lifespan. This places kra's function in the proteostasis/translational regulation axis of aging, analogous to roles described for other ribosome-associated regulatory proteins in longevity pathways.

Key pathways
translational initiation regulationribosome small subunit assembly/bindingproteostasis via mTOR-translation axis
Longevity influence
Anti-longevity
Lifespan effect
Increase

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
2/5
Failure mode
Confident wrong
Notes

The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning was plausible-sounding but ultimately incorrect — it assumed kra acts as a "translational brake" that reduces protein synthesis and thereby extends lifespan, but the actual evidence indicates kra is anti-longevity (i.e., its presence shortens lifespan or its loss extends it). The mechanistic reasoning was speculative and built on a general heuristic (reduced translation = longer life) without specific evidence for kra's actual role. The model had moderate confidence (0.62) but was wrong on both the direction and the mechanism.

Raw API responses

solver

{
  "reasoning": "The krasavietz (kra) protein binds the ribosomal small subunit and translation initiation factors, placing it as a regulator of translational initiation. In the context of aging, reduced or fine-tuned translational output — particularly through modulation of ribosome activity and initiation factor interactions — is a well-established pro-longevity mechanism in model organisms including Drosophila. By binding and potentially inhibiting or modulating translation initiation factor activity at the small ribosomal subunit, kra may act as a translational brake, reducing global protein synthesis rates and thereby alleviating proteostatic stress. Reduced translation rates are linked to decreased mTORC1 signaling output and improved proteostasis, both of which extend lifespan. This places kra's function in the proteostasis/translational regulation axis of aging, analogous to roles described for other ribosome-associated regulatory proteins in longevity pathways.",
  "confidence": 0.62,
  "key_pathways": [
    "translational initiation regulation",
    "ribosome small subunit assembly/binding",
    "proteostasis via mTOR-translation axis"
  ],
  "mechanism_class": "loss_of_proteostasis",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning was plausible-sounding but ultimately incorrect — it assumed kra acts as a \"translational brake\" that reduces protein synthesis and thereby extends lifespan, but the actual evidence indicates kra is anti-longevity (i.e., its presence shortens lifespan or its loss extends it). The mechanistic reasoning was speculative and built on a general heuristic (reduced translation = longer life) without specific evidence for kra's actual role. The model had moderate confidence (0.62) but was wrong on both the direction and the mechanism.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}
kra · Drosophila melanogaster | Aging biology eval