SCH9
S. cerevisiae
serine/threonine protein kinase SCH9
What the model saw
Gene: SCH9 Organism: Saccharomyces cerevisiae Known functions: serine/threonine protein kinase SCH9. ATP binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
View unredacted entry
serine/threonine protein kinase SCH9. ATP binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
Solver output
SCH9 is the yeast ortholog of mammalian S6 kinase (S6K1/RPS6KB1) and AKT, functioning as a central effector of the TORC1 nutrient-sensing pathway. Its serine/threonine kinase activity phosphorylates downstream targets that promote ribosome biogenesis, protein synthesis, and cell growth in response to nutrients. Deletion of SCH9 in S. cerevisiae is one of the most robust interventions known to extend chronological and replicative lifespan, acting in parallel with the Ras/PKA pathway. Active SCH9 suppresses stress-resistance transcription factors (Msn2/Msn4) and inhibits the pro-longevity kinase Rim15, thereby reducing expression of protective genes (e.g., SOD2, catalases). Thus, normal SCH9 activity drives growth at the expense of maintenance and stress resistance, a hallmark of deregulated nutrient sensing that shortens lifespan.
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 SCH9 as anti_longevity with high confidence (0.95). The mechanistic reasoning is excellent and accurate: SCH9 is indeed the yeast S6K/AKT ortholog, functions downstream of TORC1, promotes growth/protein synthesis, inhibits Rim15 and Msn2/Msn4 stress response pathways, and its deletion robustly extends both chronological and replicative lifespan. All key pathways cited are correct and well-established in the literature.
Raw API responses
solver
{
"reasoning": "SCH9 is the yeast ortholog of mammalian S6 kinase (S6K1/RPS6KB1) and AKT, functioning as a central effector of the TORC1 nutrient-sensing pathway. Its serine/threonine kinase activity phosphorylates downstream targets that promote ribosome biogenesis, protein synthesis, and cell growth in response to nutrients. Deletion of SCH9 in S. cerevisiae is one of the most robust interventions known to extend chronological and replicative lifespan, acting in parallel with the Ras/PKA pathway. Active SCH9 suppresses stress-resistance transcription factors (Msn2/Msn4) and inhibits the pro-longevity kinase Rim15, thereby reducing expression of protective genes (e.g., SOD2, catalases). Thus, normal SCH9 activity drives growth at the expense of maintenance and stress resistance, a hallmark of deregulated nutrient sensing that shortens lifespan.",
"confidence": 0.95,
"key_pathways": [
"TORC1-SCH9 nutrient sensing axis",
"Rim15-Msn2/Msn4 stress response suppression",
"Ribosome biogenesis and protein synthesis promotion"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identifies SCH9 as anti_longevity with high confidence (0.95). The mechanistic reasoning is excellent and accurate: SCH9 is indeed the yeast S6K/AKT ortholog, functions downstream of TORC1, promotes growth/protein synthesis, inhibits Rim15 and Msn2/Msn4 stress response pathways, and its deletion robustly extends both chronological and replicative lifespan. All key pathways cited are correct and well-established in the literature.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}