← Browse entries

rps-26

C. elegans

Small ribosomal subunit protein eS26

What the model saw

Gene: rps-26
Organism: Caenorhabditis elegans
Known functions: Small ribosomal subunit protein eS26. mRNA binding. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein eS26. mRNA binding. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

rps-26 encodes the small (40S) ribosomal subunit protein eS26, a structural component directly involved in mRNA binding and translation initiation. Ribosomal activity is a central downstream effector of the TOR/nutrient-sensing pathway; elevated ribosome biogenesis and translational capacity are associated with accelerated aging, while partial reduction of ribosomal subunit function (including other small-subunit proteins such as rps-11, rps-15, rps-19) extends lifespan in C. elegans by attenuating global translation rates. The normal function of rps-26 therefore promotes robust translation, which opposes longevity by sustaining high anabolic flux downstream of TOR signaling. Reduced translation fidelity or rate achieved by partial loss of ribosomal subunits also activates stress-response pathways that further contribute to lifespan extension. Thus, the wild-type pro-translational role of rps-26 is anti-longevity.

Key pathways
TOR/nutrient-sensing signalingribosome biogenesis and global translationmRNA translation initiation (40S small subunit assembly)
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
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for rps-26. The mechanistic reasoning is sound: ribosomal subunit proteins like rps-26 promote translation, and partial loss of ribosomal function extends lifespan in C. elegans by reducing global translation rates downstream of TOR signaling. The model correctly draws parallels to other small ribosomal subunit proteins (rps-11, rps-15, rps-19) that have been shown to extend lifespan when knocked down. The mechanism class "deregulated_nutrient_sensing" is reasonable though "translation/ribosome biogenesis" might be more precise. Overall, the reasoning is well-grounded and the prediction is correct with appropriate confidence (0.72).

Raw API responses

solver

{
  "reasoning": "rps-26 encodes the small (40S) ribosomal subunit protein eS26, a structural component directly involved in mRNA binding and translation initiation. Ribosomal activity is a central downstream effector of the TOR/nutrient-sensing pathway; elevated ribosome biogenesis and translational capacity are associated with accelerated aging, while partial reduction of ribosomal subunit function (including other small-subunit proteins such as rps-11, rps-15, rps-19) extends lifespan in C. elegans by attenuating global translation rates. The normal function of rps-26 therefore promotes robust translation, which opposes longevity by sustaining high anabolic flux downstream of TOR signaling. Reduced translation fidelity or rate achieved by partial loss of ribosomal subunits also activates stress-response pathways that further contribute to lifespan extension. Thus, the wild-type pro-translational role of rps-26 is anti-longevity.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR/nutrient-sensing signaling",
    "ribosome biogenesis and global translation",
    "mRNA translation initiation (40S small subunit assembly)"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for rps-26. The mechanistic reasoning is sound: ribosomal subunit proteins like rps-26 promote translation, and partial loss of ribosomal function extends lifespan in C. elegans by reducing global translation rates downstream of TOR signaling. The model correctly draws parallels to other small ribosomal subunit proteins (rps-11, rps-15, rps-19) that have been shown to extend lifespan when knocked down. The mechanism class \"deregulated_nutrient_sensing\" is reasonable though \"translation/ribosome biogenesis\" might be more precise. Overall, the reasoning is well-grounded and the prediction is correct with appropriate confidence (0.72).",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}
rps-26 · Caenorhabditis elegans | Aging biology eval