CYR1
S. cerevisiae
adenylate cyclase
What the model saw
Gene: CYR1 Organism: Saccharomyces cerevisiae Known functions: adenylate cyclase. adenylate cyclase activity. catalytic activity. magnesium ion binding. protein binding.
View unredacted entry
adenylate cyclase. adenylate cyclase activity. catalytic activity. magnesium ion binding. protein binding.
Solver output
CYR1 encodes adenylate cyclase in S. cerevisiae, the enzyme that converts ATP to cAMP, directly activating Protein Kinase A (PKA). The cAMP-PKA axis is a central nutrient-sensing pathway that, when active, suppresses stress resistance, inhibits autophagy, and promotes growth at the expense of longevity. Elevated PKA activity driven by CYR1 phosphorylates and inactivates the transcription factors Msn2/Msn4 and Rim15 kinase, thereby repressing the expression of stress-response and longevity-promoting genes. Reduced cAMP-PKA signaling (via deletion or attenuation of CYR1) is well-established to extend both chronological and replicative lifespan in yeast, phenocopying caloric restriction. Thus, the normal pro-growth function of CYR1 opposes longevity by maintaining high PKA activity and suppressing protective stress-response programs.
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 CYR1 as anti_longevity with high confidence (0.88). The mechanistic reasoning is excellent and accurate: CYR1 encodes adenylate cyclase, which produces cAMP to activate PKA, suppressing stress responses via Msn2/Msn4 and Rim15 inactivation. The model correctly notes that CYR1 deletion extends both chronological and replicative lifespan, phenocopying caloric restriction. All key pathways cited are accurate and relevant.
Raw API responses
solver
{
"reasoning": "CYR1 encodes adenylate cyclase in S. cerevisiae, the enzyme that converts ATP to cAMP, directly activating Protein Kinase A (PKA). The cAMP-PKA axis is a central nutrient-sensing pathway that, when active, suppresses stress resistance, inhibits autophagy, and promotes growth at the expense of longevity. Elevated PKA activity driven by CYR1 phosphorylates and inactivates the transcription factors Msn2/Msn4 and Rim15 kinase, thereby repressing the expression of stress-response and longevity-promoting genes. Reduced cAMP-PKA signaling (via deletion or attenuation of CYR1) is well-established to extend both chronological and replicative lifespan in yeast, phenocopying caloric restriction. Thus, the normal pro-growth function of CYR1 opposes longevity by maintaining high PKA activity and suppressing protective stress-response programs.",
"confidence": 0.88,
"key_pathways": [
"cAMP-PKA signaling",
"Msn2/Msn4 stress response",
"Rim15-Gis1 longevity pathway"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified CYR1 as anti_longevity with high confidence (0.88). The mechanistic reasoning is excellent and accurate: CYR1 encodes adenylate cyclase, which produces cAMP to activate PKA, suppressing stress responses via Msn2/Msn4 and Rim15 inactivation. The model correctly notes that CYR1 deletion extends both chronological and replicative lifespan, phenocopying caloric restriction. All key pathways cited are accurate and relevant.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}