RPL29
S. cerevisiae
60S ribosomal protein eL29 RPL29
What the model saw
Gene: RPL29 Organism: Saccharomyces cerevisiae Known functions: 60S ribosomal protein eL29 RPL29. structural constituent of ribosome.
View unredacted entry
60S ribosomal protein eL29 RPL29. structural constituent of ribosome.
Solver output
RPL29 encodes the 60S ribosomal protein eL29, a structural constituent of the large ribosomal subunit. In yeast, deletion of many large ribosomal subunit proteins (particularly 60S components) has been shown to extend chronological and replicative lifespan, likely by reducing translational capacity and mimicking dietary restriction signals through the TOR/S6K nutrient-sensing pathway. Reduced ribosome function dampens global protein synthesis rates, which attenuates TOR complex 1 (TORC1) signaling output and promotes longevity-associated responses including autophagy induction and stress resistance. The 60S subunit in particular has been linked to lifespan extension in multiple ribosomal protein deletion screens in S. cerevisiae, where loss of structural ribosomal components paradoxically extends lifespan by reducing anabolic drive.
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 based on a general pattern that deletion of 60S ribosomal proteins extends lifespan in yeast, which is true for many ribosomal proteins but not for RPL29 specifically. RPL29 is classified as anti_longevity, meaning its deletion shortens lifespan (or its presence promotes longevity). The model applied a broad heuristic incorrectly to this specific gene. The mechanistic reasoning about TOR/TORC1 and dietary restriction mimicry is plausible for other ribosomal proteins but wrong for RPL29. The model had moderate confidence (0.55) but still got the direction wrong.
Raw API responses
solver
{
"reasoning": "RPL29 encodes the 60S ribosomal protein eL29, a structural constituent of the large ribosomal subunit. In yeast, deletion of many large ribosomal subunit proteins (particularly 60S components) has been shown to extend chronological and replicative lifespan, likely by reducing translational capacity and mimicking dietary restriction signals through the TOR/S6K nutrient-sensing pathway. Reduced ribosome function dampens global protein synthesis rates, which attenuates TOR complex 1 (TORC1) signaling output and promotes longevity-associated responses including autophagy induction and stress resistance. The 60S subunit in particular has been linked to lifespan extension in multiple ribosomal protein deletion screens in S. cerevisiae, where loss of structural ribosomal components paradoxically extends lifespan by reducing anabolic drive.",
"confidence": 0.55,
"key_pathways": [
"TOR/TORC1 nutrient sensing",
"ribosome biogenesis and translational regulation",
"dietary restriction mimicry"
],
"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 based on a general pattern that deletion of 60S ribosomal proteins extends lifespan in yeast, which is true for many ribosomal proteins but not for RPL29 specifically. RPL29 is classified as anti_longevity, meaning its deletion shortens lifespan (or its presence promotes longevity). The model applied a broad heuristic incorrectly to this specific gene. The mechanistic reasoning about TOR/TORC1 and dietary restriction mimicry is plausible for other ribosomal proteins but wrong for RPL29. The model had moderate confidence (0.55) but still got the direction wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}