Myc
D. melanogaster
Myc
What the model saw
Gene: Myc Organism: Drosophila melanogaster Known functions: Myc. DNA binding. DNA-binding transcription factor activity. DNA-binding transcription factor activity, RNA polymerase II-specific. RNA polymerase II cis-regulatory region sequence-specific DNA binding. protein binding. protein dimerization activity. ubiquitin-specific protease binding.
View unredacted entry
Myc. DNA binding. DNA-binding transcription factor activity. DNA-binding transcription factor activity, RNA polymerase II-specific. RNA polymerase II cis-regulatory region sequence-specific DNA binding. protein binding. protein dimerization activity. ubiquitin-specific protease binding.
Solver output
Drosophila Myc (dMyc) is a potent RNA Pol II-specific transcription factor that drives ribosome biogenesis, protein synthesis, and cellular growth downstream of nutrient-sensing pathways including TOR/insulin signaling. By promoting anabolic transcriptional programs — including upregulation of genes involved in cell growth and proliferation — dMyc accelerates organismal growth rate at the cost of longevity, consistent with the well-established trade-off between growth/reproduction and lifespan. Its protein dimerization activity (heterodimerization with Max) is essential for binding E-box elements and activating pro-growth target genes. Overexpression of dMyc shortens lifespan in flies, while reduced dMyc activity extends lifespan, placing it functionally in opposition to longevity. The ubiquitin-specific protease binding annotation further suggests dMyc stability is regulated post-translationally, linking it to proteostatic and nutrient-sensing networks that modulate aging rate.
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 Drosophila Myc. The mechanistic reasoning is solid and well-grounded: dMyc drives ribosome biogenesis, protein synthesis, and growth programs downstream of TOR/insulin signaling, and reduced dMyc activity extends lifespan while overexpression shortens it. The Myc-Max heterodimerization and E-box binding mechanism is accurate. The classification as "deregulated_nutrient_sensing" is reasonable given dMyc's role downstream of TOR/insulin pathways, though it could also be classified under growth/proliferation signaling. The mention of ubiquitin-specific protease binding linking to proteostatic networks is a reasonable inference. Overall, the reasoning is well-articulated and mechanistically sound.
Raw API responses
solver
{
"reasoning": "Drosophila Myc (dMyc) is a potent RNA Pol II-specific transcription factor that drives ribosome biogenesis, protein synthesis, and cellular growth downstream of nutrient-sensing pathways including TOR/insulin signaling. By promoting anabolic transcriptional programs — including upregulation of genes involved in cell growth and proliferation — dMyc accelerates organismal growth rate at the cost of longevity, consistent with the well-established trade-off between growth/reproduction and lifespan. Its protein dimerization activity (heterodimerization with Max) is essential for binding E-box elements and activating pro-growth target genes. Overexpression of dMyc shortens lifespan in flies, while reduced dMyc activity extends lifespan, placing it functionally in opposition to longevity. The ubiquitin-specific protease binding annotation further suggests dMyc stability is regulated post-translationally, linking it to proteostatic and nutrient-sensing networks that modulate aging rate.",
"confidence": 0.72,
"key_pathways": [
"TOR/insulin nutrient-sensing and ribosome biogenesis",
"Myc-Max transcriptional activation of growth genes",
"E-box-dependent pro-proliferative transcription"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for Drosophila Myc. The mechanistic reasoning is solid and well-grounded: dMyc drives ribosome biogenesis, protein synthesis, and growth programs downstream of TOR/insulin signaling, and reduced dMyc activity extends lifespan while overexpression shortens it. The Myc-Max heterodimerization and E-box binding mechanism is accurate. The classification as \"deregulated_nutrient_sensing\" is reasonable given dMyc's role downstream of TOR/insulin pathways, though it could also be classified under growth/proliferation signaling. The mention of ubiquitin-specific protease binding linking to proteostatic networks is a reasonable inference. Overall, the reasoning is well-articulated and mechanistically sound.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}