APT1
S. cerevisiae
adenine phosphoribosyltransferase APT1
What the model saw
Gene: APT1 Organism: Saccharomyces cerevisiae Known functions: adenine phosphoribosyltransferase APT1. AMP binding. adenine binding. adenine phosphoribosyltransferase activity. protein binding.
View unredacted entry
adenine phosphoribosyltransferase APT1. AMP binding. adenine binding. adenine phosphoribosyltransferase activity. protein binding.
Solver output
APT1 encodes adenine phosphoribosyltransferase, which catalyzes the salvage of adenine into AMP by transferring adenine onto phosphoribosyl pyrophosphate (PRPP). This salvage pathway recycles purine bases, maintaining the intracellular adenine/AMP pool without the energetic cost of de novo purine synthesis. Adequate AMP levels support AMPK (Snf1 in yeast) activation, a key nutrient-sensing kinase that promotes longevity through downstream effects on autophagy and metabolic homeostasis. Additionally, efficient purine recycling reduces the accumulation of potentially toxic purine catabolites and supports NAD+ precursor metabolism, both relevant to aging. Loss of APT1 function would impair purine salvage, potentially depleting AMP pools and disrupting energy sensing, which is generally detrimental to 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 predicted pro_longevity but the ground truth is anti_longevity. APT1 is anti-longevity, meaning its deletion or loss extends lifespan, not reduces it. The model's reasoning was speculative and built a plausible-sounding but incorrect mechanistic story about AMP/AMPK signaling supporting longevity. The model concluded that loss of APT1 would be detrimental to lifespan, which is the opposite of what the GenAge database records. The model had moderate confidence (0.62) but was wrong on both the answer and the mechanism.
Raw API responses
solver
{
"reasoning": "APT1 encodes adenine phosphoribosyltransferase, which catalyzes the salvage of adenine into AMP by transferring adenine onto phosphoribosyl pyrophosphate (PRPP). This salvage pathway recycles purine bases, maintaining the intracellular adenine/AMP pool without the energetic cost of de novo purine synthesis. Adequate AMP levels support AMPK (Snf1 in yeast) activation, a key nutrient-sensing kinase that promotes longevity through downstream effects on autophagy and metabolic homeostasis. Additionally, efficient purine recycling reduces the accumulation of potentially toxic purine catabolites and supports NAD+ precursor metabolism, both relevant to aging. Loss of APT1 function would impair purine salvage, potentially depleting AMP pools and disrupting energy sensing, which is generally detrimental to lifespan.",
"confidence": 0.62,
"key_pathways": [
"purine salvage pathway",
"AMP/AMPK (Snf1) nutrient sensing",
"nucleotide metabolism"
],
"mechanism_class": "other",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. APT1 is anti-longevity, meaning its deletion or loss extends lifespan, not reduces it. The model's reasoning was speculative and built a plausible-sounding but incorrect mechanistic story about AMP/AMPK signaling supporting longevity. The model concluded that loss of APT1 would be detrimental to lifespan, which is the opposite of what the GenAge database records. The model had moderate confidence (0.62) but was wrong on both the answer and the mechanism.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}