rpsa-1
C. elegans
Small ribosomal subunit protein uS2
What the model saw
Gene: rpsa-1 Organism: Caenorhabditis elegans Known functions: Small ribosomal subunit protein uS2. protein binding. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein uS2. protein binding. structural constituent of ribosome.
Solver output
rpsa-1 encodes the small ribosomal subunit protein uS2, a core structural component of the 40S ribosomal subunit required for mRNA translation initiation and global protein synthesis. Ribosomal activity is tightly coupled to nutrient-sensing pathways, particularly TOR (mTORC1) signaling, which upregulates ribosome biogenesis and translational output in nutrient-rich conditions. In C. elegans, reduced ribosomal function — through partial loss-of-function of small subunit proteins — is well-established to extend lifespan, likely by mimicking dietary restriction and dampening mTOR-driven anabolic signaling. The normal (full) function of rpsa-1 therefore sustains high translational capacity, promoting growth and reproduction at the expense of longevity. This is consistent with the broader finding that ribosomal protein knockdowns (e.g., rps-6, rps-11) extend lifespan in worms via reduced protein synthesis and activation of stress-response pathways.
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 rpsa-1. The mechanistic reasoning is sound: rpsa-1 encodes a small ribosomal subunit protein (uS2/40S), and reduced ribosomal function in C. elegans is well-established to extend lifespan, making the normal function of rpsa-1 anti-longevity. The model correctly connects this to TOR/nutrient-sensing pathways and dietary restriction mimicry, and cites relevant analogous ribosomal protein knockdowns. The mechanism class "deregulated_nutrient_sensing" is a reasonable (if slightly imprecise) categorization — the more direct mechanism is reduced protein synthesis/translational capacity, but TOR signaling is indeed closely linked. Confidence of 0.72 is appropriate given the indirect inference from gene function. Overall a well-reasoned, correct prediction.
Raw API responses
solver
{
"reasoning": "rpsa-1 encodes the small ribosomal subunit protein uS2, a core structural component of the 40S ribosomal subunit required for mRNA translation initiation and global protein synthesis. Ribosomal activity is tightly coupled to nutrient-sensing pathways, particularly TOR (mTORC1) signaling, which upregulates ribosome biogenesis and translational output in nutrient-rich conditions. In C. elegans, reduced ribosomal function — through partial loss-of-function of small subunit proteins — is well-established to extend lifespan, likely by mimicking dietary restriction and dampening mTOR-driven anabolic signaling. The normal (full) function of rpsa-1 therefore sustains high translational capacity, promoting growth and reproduction at the expense of longevity. This is consistent with the broader finding that ribosomal protein knockdowns (e.g., rps-6, rps-11) extend lifespan in worms via reduced protein synthesis and activation of stress-response pathways.",
"confidence": 0.72,
"key_pathways": [
"mTOR/TOR nutrient-sensing and ribosome biogenesis",
"translational regulation and protein synthesis",
"dietary restriction mimicry via reduced ribosomal activity"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for rpsa-1. The mechanistic reasoning is sound: rpsa-1 encodes a small ribosomal subunit protein (uS2/40S), and reduced ribosomal function in C. elegans is well-established to extend lifespan, making the normal function of rpsa-1 anti-longevity. The model correctly connects this to TOR/nutrient-sensing pathways and dietary restriction mimicry, and cites relevant analogous ribosomal protein knockdowns. The mechanism class \"deregulated_nutrient_sensing\" is a reasonable (if slightly imprecise) categorization — the more direct mechanism is reduced protein synthesis/translational capacity, but TOR signaling is indeed closely linked. Confidence of 0.72 is appropriate given the indirect inference from gene function. Overall a well-reasoned, correct prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}