rps-8
C. elegans
Small ribosomal subunit protein eS8
What the model saw
Gene: rps-8 Organism: Caenorhabditis elegans Known functions: Small ribosomal subunit protein eS8. structural constituent of ribosome.
View unredacted entry
Small ribosomal subunit protein eS8. structural constituent of ribosome.
Solver output
rps-8 encodes the small ribosomal subunit protein eS8, a structural component of the 40S ribosome. In C. elegans, partial loss-of-function of ribosomal small subunit proteins (including rps genes) has been shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/mTORC1 signaling — a key nutrient-sensing pathway linked to longevity. Reduced ribosomal activity lowers the production of pro-aging proteins while potentially upregulating stress-response and proteostasis pathways. However, the normal (wild-type) function of rps-8 is to sustain full translational capacity, which supports growth and reproduction but is associated with a shorter lifespan. Thus, the gene's normal function — promoting maximal ribosome activity and translation — is anti-longevity in the context of aging biology, as its reduction (not its presence) confers 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 predicted "pro_longevity" but the ground truth is "anti_longevity." The model's reasoning is internally contradictory and ultimately confused. It correctly identifies that reducing ribosomal subunit activity can extend lifespan, but then concludes the gene is "pro_longevity" — when in fact, if knockdown/reduction extends lifespan, the gene's normal function is anti-longevity (it promotes aging/shortens lifespan). The model even states in its own reasoning: "the gene's normal function — promoting maximal ribosome activity and translation — is anti-longevity in the context of aging biology," which is the correct conclusion, yet it still labeled the gene as "pro_longevity." This is a direct self-contradiction. The mechanism class of "deregulated_nutrient_sensing" is also not the most accurate framing — the primary mechanism is translational regulation/ribosome function. The model's final label is wrong despite partially correct mechanistic reasoning, and the confidence of 0.65 is too high given the confusion.
Raw API responses
solver
{
"reasoning": "rps-8 encodes the small ribosomal subunit protein eS8, a structural component of the 40S ribosome. In C. elegans, partial loss-of-function of ribosomal small subunit proteins (including rps genes) has been shown to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/mTORC1 signaling — a key nutrient-sensing pathway linked to longevity. Reduced ribosomal activity lowers the production of pro-aging proteins while potentially upregulating stress-response and proteostasis pathways. However, the normal (wild-type) function of rps-8 is to sustain full translational capacity, which supports growth and reproduction but is associated with a shorter lifespan. Thus, the gene's normal function — promoting maximal ribosome activity and translation — is anti-longevity in the context of aging biology, as its reduction (not its presence) confers lifespan extension.",
"confidence": 0.65,
"key_pathways": [
"mTOR/TOR nutrient-sensing and translation regulation",
"ribosome biogenesis and global protein synthesis",
"dietary restriction mimicry via reduced translational output"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted \"pro_longevity\" but the ground truth is \"anti_longevity.\" The model's reasoning is internally contradictory and ultimately confused. It correctly identifies that reducing ribosomal subunit activity can extend lifespan, but then concludes the gene is \"pro_longevity\" — when in fact, if knockdown/reduction extends lifespan, the gene's normal function is anti-longevity (it promotes aging/shortens lifespan). The model even states in its own reasoning: \"the gene's normal function — promoting maximal ribosome activity and translation — is anti-longevity in the context of aging biology,\" which is the correct conclusion, yet it still labeled the gene as \"pro_longevity.\" This is a direct self-contradiction. The mechanism class of \"deregulated_nutrient_sensing\" is also not the most accurate framing — the primary mechanism is translational regulation/ribosome function. The model's final label is wrong despite partially correct mechanistic reasoning, and the confidence of 0.65 is too high given the confusion.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}