rpl-17
C. elegans
Large ribosomal subunit protein uL22
What the model saw
Gene: rpl-17 Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein uL22. structural constituent of ribosome.
View unredacted entry
Large ribosomal subunit protein uL22. structural constituent of ribosome.
Solver output
rpl-17 encodes the large ribosomal subunit protein uL22, a structural component of the 60S ribosomal subunit. In C. elegans, partial loss-of-function of large ribosomal subunit proteins (including multiple RPL genes) is well-documented to extend lifespan, acting through reduced translational capacity that mimics dietary restriction and downregulates TOR/TORC1 signaling. Reduced ribosome activity lowers global protein synthesis rates, which feeds back into nutrient-sensing pathways (TOR, IIS) to promote longevity. Thus, the normal function of rpl-17 — supporting full ribosomal translation — opposes the longevity benefit seen when this pathway is attenuated. However, the gene's normal function (promoting translation) is anti-longevity in this context, as its reduction extends lifespan via decreased TOR-driven protein synthesis.
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 identifies the mechanism — that rpl-17 encodes a large ribosomal subunit protein, and that reduction of ribosomal proteins in C. elegans extends lifespan via reduced translation/TOR signaling. However, the model contradicts itself and ultimately outputs the wrong answer. The model's reasoning explicitly states "the gene's normal function (promoting translation) is anti-longevity," which aligns with the ground truth (anti_longevity). But the final prediction field says "pro_longevity," which is incorrect. The model seems confused about the directionality convention: it correctly understands that loss of rpl-17 extends lifespan (making the gene anti-longevity in its normal function), but then labels it "pro_longevity" — possibly confusing the effect of the knockdown with the gene's classification. The mechanistic reasoning is largely correct, but the final answer label is wrong.
Raw API responses
solver
{
"reasoning": "rpl-17 encodes the large ribosomal subunit protein uL22, a structural component of the 60S ribosomal subunit. In C. elegans, partial loss-of-function of large ribosomal subunit proteins (including multiple RPL genes) is well-documented to extend lifespan, acting through reduced translational capacity that mimics dietary restriction and downregulates TOR/TORC1 signaling. Reduced ribosome activity lowers global protein synthesis rates, which feeds back into nutrient-sensing pathways (TOR, IIS) to promote longevity. Thus, the normal function of rpl-17 — supporting full ribosomal translation — opposes the longevity benefit seen when this pathway is attenuated. However, the gene's normal function (promoting translation) is anti-longevity in this context, as its reduction extends lifespan via decreased TOR-driven protein synthesis.",
"confidence": 0.72,
"key_pathways": [
"TOR/TORC1 nutrient sensing",
"ribosomal translation regulation",
"dietary restriction mimicry"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identifies the mechanism — that rpl-17 encodes a large ribosomal subunit protein, and that reduction of ribosomal proteins in C. elegans extends lifespan via reduced translation/TOR signaling. However, the model contradicts itself and ultimately outputs the wrong answer. The model's reasoning explicitly states \"the gene's normal function (promoting translation) is anti-longevity,\" which aligns with the ground truth (anti_longevity). But the final prediction field says \"pro_longevity,\" which is incorrect. The model seems confused about the directionality convention: it correctly understands that loss of rpl-17 extends lifespan (making the gene anti-longevity in its normal function), but then labels it \"pro_longevity\" — possibly confusing the effect of the knockdown with the gene's classification. The mechanistic reasoning is largely correct, but the final answer label is wrong.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}