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mrpl-12

C. elegans

Mitochondrial Ribosomal Protein, Large

What the model saw

Gene: mrpl-12
Organism: Caenorhabditis elegans
Known functions: Mitochondrial Ribosomal Protein, Large. mRNA binding. protein binding. structural constituent of ribosome.
View unredacted entry
Mitochondrial Ribosomal Protein, Large. mRNA binding. protein binding. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Mitochondrial dysfunction
Reasoning

mrpl-12 encodes a large subunit mitochondrial ribosomal protein responsible for mitochondrial translation. Mitochondrial ribosomes synthesize the 13 core subunits of the oxidative phosphorylation (OXPHOS) complexes encoded by mtDNA. In C. elegans, RNAi knockdown of mitochondrial ribosomal proteins (including mrpl genes) has been shown to extend lifespan, consistent with the broader finding that mild impairment of mitochondrial translation reduces OXPHOS activity and reactive oxygen species (ROS) production, mimicking a caloric restriction-like state. The normal (wild-type) function of mrpl-12 therefore promotes full mitochondrial translation and OXPHOS output, which is associated with shorter lifespan in this organism. This places mrpl-12 in the category of genes whose normal activity opposes longevity, acting through the mitochondrial dysfunction/mitohormesis axis rather than through a protective role.

Key pathways
mitochondrial translationoxidative phosphorylation (OXPHOS)mitohormesis / ROS signaling
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
5/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for mrpl-12 in C. elegans. The mechanistic reasoning is sound and well-articulated: mrpl-12 encodes a mitochondrial large ribosomal subunit protein involved in mitochondrial translation; RNAi knockdown of such genes extends lifespan in C. elegans through mild mitochondrial impairment/mitohormesis. The model correctly identifies that the wild-type function of mrpl-12 promotes full OXPHOS output, which is associated with shorter lifespan, making it anti-longevity. The confidence level (0.72) is appropriate given the general knowledge about mrpl genes in C. elegans. All key pathways identified are relevant and correct.

Raw API responses

solver

{
  "reasoning": "mrpl-12 encodes a large subunit mitochondrial ribosomal protein responsible for mitochondrial translation. Mitochondrial ribosomes synthesize the 13 core subunits of the oxidative phosphorylation (OXPHOS) complexes encoded by mtDNA. In C. elegans, RNAi knockdown of mitochondrial ribosomal proteins (including mrpl genes) has been shown to extend lifespan, consistent with the broader finding that mild impairment of mitochondrial translation reduces OXPHOS activity and reactive oxygen species (ROS) production, mimicking a caloric restriction-like state. The normal (wild-type) function of mrpl-12 therefore promotes full mitochondrial translation and OXPHOS output, which is associated with shorter lifespan in this organism. This places mrpl-12 in the category of genes whose normal activity opposes longevity, acting through the mitochondrial dysfunction/mitohormesis axis rather than through a protective role.",
  "confidence": 0.72,
  "key_pathways": [
    "mitochondrial translation",
    "oxidative phosphorylation (OXPHOS)",
    "mitohormesis / ROS signaling"
  ],
  "mechanism_class": "mitochondrial_dysfunction",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for mrpl-12 in C. elegans. The mechanistic reasoning is sound and well-articulated: mrpl-12 encodes a mitochondrial large ribosomal subunit protein involved in mitochondrial translation; RNAi knockdown of such genes extends lifespan in C. elegans through mild mitochondrial impairment/mitohormesis. The model correctly identifies that the wild-type function of mrpl-12 promotes full OXPHOS output, which is associated with shorter lifespan, making it anti-longevity. The confidence level (0.72) is appropriate given the general knowledge about mrpl genes in C. elegans. All key pathways identified are relevant and correct.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}