SNF1
S. cerevisiae
AMP-activated serine/threonine-protein kinase catalytic subunit SNF1
What the model saw
Gene: SNF1 Organism: Saccharomyces cerevisiae Known functions: AMP-activated serine/threonine-protein kinase catalytic subunit SNF1. AMP-activated protein kinase activity. ATP binding. guanyl-nucleotide exchange factor activity. identical protein binding. molecular function activator activity. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
View unredacted entry
AMP-activated serine/threonine-protein kinase catalytic subunit SNF1. AMP-activated protein kinase activity. ATP binding. guanyl-nucleotide exchange factor activity. identical protein binding. molecular function activator activity. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
Solver output
SNF1 is the yeast ortholog of mammalian AMP-activated protein kinase (AMPK), a master energy sensor that is activated under low-energy/nutrient-limiting conditions. As a serine/threonine kinase activated by AMP, SNF1 phosphorylates and inhibits key anabolic targets while activating catabolic processes, mimicking the beneficial effects of caloric restriction. SNF1/AMPK activation suppresses TORC1 signaling and promotes autophagy, both of which are well-established pro-longevity mechanisms in yeast and other organisms. In S. cerevisiae, SNF1 activity is required for chronological and replicative lifespan extension under glucose limitation, and its loss shortens lifespan. The guanyl-nucleotide exchange factor activity annotation may reflect upstream regulatory interactions, but the dominant pro-longevity role is through AMPK-mediated nutrient sensing and metabolic reprogramming.
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 predicted pro_longevity with high confidence (0.88), but the ground truth is anti_longevity. The model's reasoning follows a plausible but incorrect narrative: while AMPK/SNF1 is indeed a master energy sensor and its activation does mimic caloric restriction in many contexts, in S. cerevisiae SNF1 actually has an anti-longevity role. The model correctly identifies SNF1 as the yeast AMPK ortholog and correctly describes its biochemical functions, but draws the wrong conclusion about its net effect on lifespan. In yeast, SNF1 has been shown to promote aging rather than extend lifespan - for example, SNF1 activity can promote chronological aging through mechanisms including activation of stress responses that paradoxically shorten lifespan, or through effects on acetic acid production. The model's reasoning is internally coherent but based on an oversimplified extrapolation from mammalian AMPK biology to yeast SNF1 longevity effects, ignoring the organism-specific nuances that make SNF1 anti-longevity in S. cerevisiae.
Raw API responses
solver
{
"reasoning": "SNF1 is the yeast ortholog of mammalian AMP-activated protein kinase (AMPK), a master energy sensor that is activated under low-energy/nutrient-limiting conditions. As a serine/threonine kinase activated by AMP, SNF1 phosphorylates and inhibits key anabolic targets while activating catabolic processes, mimicking the beneficial effects of caloric restriction. SNF1/AMPK activation suppresses TORC1 signaling and promotes autophagy, both of which are well-established pro-longevity mechanisms in yeast and other organisms. In S. cerevisiae, SNF1 activity is required for chronological and replicative lifespan extension under glucose limitation, and its loss shortens lifespan. The guanyl-nucleotide exchange factor activity annotation may reflect upstream regulatory interactions, but the dominant pro-longevity role is through AMPK-mediated nutrient sensing and metabolic reprogramming.",
"confidence": 0.88,
"key_pathways": [
"AMPK/SNF1 nutrient sensing pathway",
"TORC1 inhibition and caloric restriction mimicry",
"Autophagy induction under energy stress"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity with high confidence (0.88), but the ground truth is anti_longevity. The model's reasoning follows a plausible but incorrect narrative: while AMPK/SNF1 is indeed a master energy sensor and its activation does mimic caloric restriction in many contexts, in S. cerevisiae SNF1 actually has an anti-longevity role. The model correctly identifies SNF1 as the yeast AMPK ortholog and correctly describes its biochemical functions, but draws the wrong conclusion about its net effect on lifespan. In yeast, SNF1 has been shown to promote aging rather than extend lifespan - for example, SNF1 activity can promote chronological aging through mechanisms including activation of stress responses that paradoxically shorten lifespan, or through effects on acetic acid production. The model's reasoning is internally coherent but based on an oversimplified extrapolation from mammalian AMPK biology to yeast SNF1 longevity effects, ignoring the organism-specific nuances that make SNF1 anti-longevity in S. cerevisiae.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}