rpc-2
C. elegans
DNA-directed RNA polymerase subunit beta
What the model saw
Gene: rpc-2 Organism: Caenorhabditis elegans Known functions: DNA-directed RNA polymerase subunit beta. 5'-3' RNA polymerase activity. DNA binding. DNA-directed RNA polymerase activity. ribonucleoside binding.
View unredacted entry
DNA-directed RNA polymerase subunit beta. 5'-3' RNA polymerase activity. DNA binding. DNA-directed RNA polymerase activity. ribonucleoside binding.
Solver output
rpc-2 encodes the beta subunit of DNA-directed RNA Polymerase III (Pol III), which is responsible for transcribing small non-coding RNAs including tRNAs, 5S rRNA, and other structural RNAs essential for protein synthesis capacity. In C. elegans and other organisms, reduced Pol III activity has been linked to lifespan extension, as downregulation of tRNA biogenesis and ribosome biogenesis pathways intersects with nutrient-sensing (TOR/mTORC1) signaling to promote longevity. However, the normal (wild-type) function of rpc-2 is to sustain Pol III transcription, which supports robust translation and growth — processes that when overactive are associated with shortened lifespan via deregulated nutrient sensing. The normal pro-growth role of Pol III activity thus opposes longevity, placing rpc-2 in the anti-longevity category; yet because Pol III is also required for cellular homeostasis and proteostasis, the picture is nuanced. Given that Pol III activity is a known downstream effector of TORC1 and its reduction extends lifespan in multiple organisms, the wild-type function of rpc-2 is best classified as anti-longevity through the deregulated nutrient-sensing hallmark.
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 identified the mechanistic framework (Pol III activity, TOR/mTORC1 signaling, tRNA biogenesis) and even explicitly stated "the wild-type function of rpc-2 is best classified as anti-longevity" in its reasoning. However, the final prediction output was "pro_longevity" — the opposite of both the ground truth (anti_longevity) and the model's own stated conclusion in the reasoning text. This is a contradiction between the reasoning and the final answer. The model's reasoning correctly identifies rpc-2 as anti-longevity (supporting growth/translation that opposes longevity), but the JSON output says "pro_longevity" with 0.62 confidence. This appears to be an error in translating the reasoning into the final answer field. The mechanism class "epigenetic_alterations" is also somewhat inaccurate — Pol III transcription is more accurately classified under translational regulation or nutrient sensing rather than epigenetic alterations.
Raw API responses
solver
{
"reasoning": "rpc-2 encodes the beta subunit of DNA-directed RNA Polymerase III (Pol III), which is responsible for transcribing small non-coding RNAs including tRNAs, 5S rRNA, and other structural RNAs essential for protein synthesis capacity. In C. elegans and other organisms, reduced Pol III activity has been linked to lifespan extension, as downregulation of tRNA biogenesis and ribosome biogenesis pathways intersects with nutrient-sensing (TOR/mTORC1) signaling to promote longevity. However, the normal (wild-type) function of rpc-2 is to sustain Pol III transcription, which supports robust translation and growth — processes that when overactive are associated with shortened lifespan via deregulated nutrient sensing. The normal pro-growth role of Pol III activity thus opposes longevity, placing rpc-2 in the anti-longevity category; yet because Pol III is also required for cellular homeostasis and proteostasis, the picture is nuanced. Given that Pol III activity is a known downstream effector of TORC1 and its reduction extends lifespan in multiple organisms, the wild-type function of rpc-2 is best classified as anti-longevity through the deregulated nutrient-sensing hallmark.",
"confidence": 0.62,
"key_pathways": [
"RNA Polymerase III / tRNA biogenesis",
"TOR/mTORC1 nutrient-sensing signaling",
"ribosome biogenesis and translational capacity"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identified the mechanistic framework (Pol III activity, TOR/mTORC1 signaling, tRNA biogenesis) and even explicitly stated \"the wild-type function of rpc-2 is best classified as anti-longevity\" in its reasoning. However, the final prediction output was \"pro_longevity\" — the opposite of both the ground truth (anti_longevity) and the model's own stated conclusion in the reasoning text. This is a contradiction between the reasoning and the final answer. The model's reasoning correctly identifies rpc-2 as anti-longevity (supporting growth/translation that opposes longevity), but the JSON output says \"pro_longevity\" with 0.62 confidence. This appears to be an error in translating the reasoning into the final answer field. The mechanism class \"epigenetic_alterations\" is also somewhat inaccurate — Pol III transcription is more accurately classified under translational regulation or nutrient sensing rather than epigenetic alterations.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}