mrps-30
C. elegans
Mitochondrial Ribosomal Protein, Small
What the model saw
Gene: mrps-30 Organism: Caenorhabditis elegans Known functions: Mitochondrial Ribosomal Protein, Small. structural constituent of ribosome.
View unredacted entry
Mitochondrial Ribosomal Protein, Small. structural constituent of ribosome.
Solver output
mrps-30 encodes a small subunit protein of the mitochondrial ribosome, which is required for translation of the 13 mitochondrially-encoded subunits of the oxidative phosphorylation complexes. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (including mrps subunits) has been shown to reduce mitochondrial translation and OXPHOS activity, which paradoxically extends lifespan via the mitochondrial unfolded protein response (UPRmt) and reduced ROS production — a phenomenon well-documented in the "mitochondrial hormesis" framework. However, the normal (wild-type) function of mrps-30 is to sustain full mitochondrial translation capacity, which supports high OXPHOS activity and ATP production but also drives elevated ROS and accelerates aging. Thus, the gene's normal function — promoting efficient mitochondrial protein synthesis — is anti-longevity, as its reduction (not its presence) is what extends lifespan in multiple studies on mitochondrial ribosomal components in C. elegans.
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 correctly predicted anti_longevity for mrps-30. The mechanistic reasoning is sound: mrps-30 encodes a mitochondrial small ribosomal subunit protein, and its normal function promotes mitochondrial translation/OXPHOS, which drives aging. Knockdown/loss of mrps-30 extends lifespan via mitochondrial hormesis/UPRmt, making the gene's normal function anti-longevity. The reasoning about mitochondrial ribosomal proteins in C. elegans is well-established in the literature. Confidence of 0.65 is appropriately calibrated. Minor note: the model could have been slightly more specific about the actual experimental evidence for mrps-30 specifically vs. generalizing from other mrps genes, but the overall framework is correct.
Raw API responses
solver
{
"reasoning": "mrps-30 encodes a small subunit protein of the mitochondrial ribosome, which is required for translation of the 13 mitochondrially-encoded subunits of the oxidative phosphorylation complexes. In C. elegans, partial loss-of-function of mitochondrial ribosomal proteins (including mrps subunits) has been shown to reduce mitochondrial translation and OXPHOS activity, which paradoxically extends lifespan via the mitochondrial unfolded protein response (UPRmt) and reduced ROS production — a phenomenon well-documented in the \"mitochondrial hormesis\" framework. However, the normal (wild-type) function of mrps-30 is to sustain full mitochondrial translation capacity, which supports high OXPHOS activity and ATP production but also drives elevated ROS and accelerates aging. Thus, the gene's normal function — promoting efficient mitochondrial protein synthesis — is anti-longevity, as its reduction (not its presence) is what extends lifespan in multiple studies on mitochondrial ribosomal components in C. elegans.",
"confidence": 0.65,
"key_pathways": [
"mitochondrial translation / OXPHOS",
"mitochondrial unfolded protein response (UPRmt)",
"reactive oxygen species (ROS) signaling"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for mrps-30. The mechanistic reasoning is sound: mrps-30 encodes a mitochondrial small ribosomal subunit protein, and its normal function promotes mitochondrial translation/OXPHOS, which drives aging. Knockdown/loss of mrps-30 extends lifespan via mitochondrial hormesis/UPRmt, making the gene's normal function anti-longevity. The reasoning about mitochondrial ribosomal proteins in C. elegans is well-established in the literature. Confidence of 0.65 is appropriately calibrated. Minor note: the model could have been slightly more specific about the actual experimental evidence for mrps-30 specifically vs. generalizing from other mrps genes, but the overall framework is correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}