RAS1
S. cerevisiae
Ras family GTPase RAS1
What the model saw
Gene: RAS1 Organism: Saccharomyces cerevisiae Known functions: Ras family GTPase RAS1. G protein activity. GTP binding. GTPase activity.
View unredacted entry
Ras family GTPase RAS1. G protein activity. GTP binding. GTPase activity.
Solver output
RAS1 encodes a Ras family GTPase in S. cerevisiae that activates adenylyl cyclase (Cyr1) via GTP-bound active state, elevating cAMP levels and stimulating PKA (protein kinase A) activity. Hyperactive Ras/PKA signaling suppresses stress response transcription factors (Msn2/Msn4), inhibits autophagy, and promotes anabolic growth at the expense of stress resistance and longevity. In yeast chronological and replicative aging models, attenuation of Ras/cAMP/PKA signaling — analogous to reduced IGF-1/insulin signaling in metazoans — is a well-established pro-longevity intervention. RAS1's normal GTPase activity (cycling between active GTP-bound and inactive GDP-bound states) drives nutrient-sensing growth programs that, when sustained, shorten lifespan. Loss-of-function ras1 mutants or dominant-negative alleles extend both chronological and replicative lifespan in yeast, confirming the anti-longevity role of normal RAS1 function.
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 RAS1 as anti_longevity with high confidence (0.88). The mechanistic reasoning is thorough and accurate: RAS1 activates adenylyl cyclase (Cyr1), elevating cAMP and PKA activity, which suppresses stress response transcription factors (Msn2/Msn4), inhibits autophagy, and promotes growth at the expense of stress resistance. The model correctly notes that loss-of-function ras1 mutants extend lifespan, confirming the anti-longevity role. The pathway classification as "deregulated_nutrient_sensing" is appropriate. The reasoning is well-grounded in established yeast aging biology.
Raw API responses
solver
{
"reasoning": "RAS1 encodes a Ras family GTPase in S. cerevisiae that activates adenylyl cyclase (Cyr1) via GTP-bound active state, elevating cAMP levels and stimulating PKA (protein kinase A) activity. Hyperactive Ras/PKA signaling suppresses stress response transcription factors (Msn2/Msn4), inhibits autophagy, and promotes anabolic growth at the expense of stress resistance and longevity. In yeast chronological and replicative aging models, attenuation of Ras/cAMP/PKA signaling — analogous to reduced IGF-1/insulin signaling in metazoans — is a well-established pro-longevity intervention. RAS1's normal GTPase activity (cycling between active GTP-bound and inactive GDP-bound states) drives nutrient-sensing growth programs that, when sustained, shorten lifespan. Loss-of-function ras1 mutants or dominant-negative alleles extend both chronological and replicative lifespan in yeast, confirming the anti-longevity role of normal RAS1 function.",
"confidence": 0.88,
"key_pathways": [
"Ras/cAMP/PKA nutrient-sensing pathway",
"Msn2/Msn4 stress response suppression",
"Autophagy inhibition via PKA"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified RAS1 as anti_longevity with high confidence (0.88). The mechanistic reasoning is thorough and accurate: RAS1 activates adenylyl cyclase (Cyr1), elevating cAMP and PKA activity, which suppresses stress response transcription factors (Msn2/Msn4), inhibits autophagy, and promotes growth at the expense of stress resistance. The model correctly notes that loss-of-function ras1 mutants extend lifespan, confirming the anti-longevity role. The pathway classification as \"deregulated_nutrient_sensing\" is appropriate. The reasoning is well-grounded in established yeast aging biology.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}