rps-10
C. elegans
Plectin/eS10 N-terminal domain-containing protein
What the model saw
Gene: rps-10 Organism: Caenorhabditis elegans Known functions: Plectin/eS10 N-terminal domain-containing protein. RNA binding. protein binding. structural constituent of ribosome.
View unredacted entry
Plectin/eS10 N-terminal domain-containing protein. RNA binding. protein binding. structural constituent of ribosome.
Solver output
rps-10 encodes the small ribosomal subunit protein eS10 (RPS10), a structural constituent of the 40S ribosome. Ribosomal protein genes in C. elegans are well-established modulators of longevity: partial loss-of-function of small subunit ribosomal proteins (e.g., rps-6, rps-11) consistently extends lifespan by reducing global translational capacity, which mimics dietary restriction and downregulates mTORC1/S6K-mediated nutrient sensing. The structural role of RPS-10 in ribosome assembly means its normal function sustains high translational output, which promotes growth and reproduction at the cost of longevity. Reduced ribosomal activity is linked to activation of stress-response transcription factors (e.g., DAF-16/FOXO, PHA-4/FOXA) and enhanced proteostasis, further supporting lifespan extension when this gene's function is diminished. Therefore, the normal (wild-type) function of rps-10 is anti-longevity, as it maintains the elevated translation rate that opposes lifespan extension.
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 rps-10. The mechanistic reasoning is sound: ribosomal protein genes in C. elegans are well-established anti-longevity factors, where knockdown of small subunit ribosomal proteins extends lifespan by reducing translational capacity, mimicking dietary restriction. The model correctly identifies the role of mTORC1/S6K signaling, DAF-16/FOXO, and PHA-4/FOXA pathways. The reasoning is well-grounded in the literature on ribosomal protein knockdowns in C. elegans. Confidence of 0.72 is appropriate given the gene-specific uncertainty. Minor note: the model generalizes from other rps genes (rps-6, rps-11) to rps-10, which is reasonable but slightly indirect.
Raw API responses
solver
{
"reasoning": "rps-10 encodes the small ribosomal subunit protein eS10 (RPS10), a structural constituent of the 40S ribosome. Ribosomal protein genes in C. elegans are well-established modulators of longevity: partial loss-of-function of small subunit ribosomal proteins (e.g., rps-6, rps-11) consistently extends lifespan by reducing global translational capacity, which mimics dietary restriction and downregulates mTORC1/S6K-mediated nutrient sensing. The structural role of RPS-10 in ribosome assembly means its normal function sustains high translational output, which promotes growth and reproduction at the cost of longevity. Reduced ribosomal activity is linked to activation of stress-response transcription factors (e.g., DAF-16/FOXO, PHA-4/FOXA) and enhanced proteostasis, further supporting lifespan extension when this gene's function is diminished. Therefore, the normal (wild-type) function of rps-10 is anti-longevity, as it maintains the elevated translation rate that opposes lifespan extension.",
"confidence": 0.72,
"key_pathways": [
"mTORC1/S6K translational regulation",
"ribosome biogenesis and global protein synthesis",
"dietary restriction mimicry via reduced translational capacity"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for rps-10. The mechanistic reasoning is sound: ribosomal protein genes in C. elegans are well-established anti-longevity factors, where knockdown of small subunit ribosomal proteins extends lifespan by reducing translational capacity, mimicking dietary restriction. The model correctly identifies the role of mTORC1/S6K signaling, DAF-16/FOXO, and PHA-4/FOXA pathways. The reasoning is well-grounded in the literature on ribosomal protein knockdowns in C. elegans. Confidence of 0.72 is appropriate given the gene-specific uncertainty. Minor note: the model generalizes from other rps genes (rps-6, rps-11) to rps-10, which is reasonable but slightly indirect.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}