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BNA6

S. cerevisiae

nicotinate-nucleotide diphosphorylase (carboxylating)

What the model saw

Gene: BNA6
Organism: Saccharomyces cerevisiae
Known functions: nicotinate-nucleotide diphosphorylase (carboxylating). nicotinate-nucleotide diphosphorylase (carboxylating) activity. pentosyltransferase activity.
View unredacted entry
nicotinate-nucleotide diphosphorylase (carboxylating). nicotinate-nucleotide diphosphorylase (carboxylating) activity. pentosyltransferase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

BNA6 encodes nicotinate-nucleotide diphosphorylase (carboxylating), which catalyzes the penultimate step in the de novo NAD⁺ biosynthesis pathway (the kynurenine/tryptophan pathway) in yeast, converting quinolinate to nicotinate mononucleotide (NaMN). NAD⁺ is a critical coenzyme and signaling molecule whose intracellular levels directly regulate the activity of Sir2/sirtuins, the yeast NAD⁺-dependent deacetylases that are central mediators of caloric restriction-induced longevity. By contributing to NAD⁺ biosynthesis, BNA6 supports sirtuin activity, which in turn promotes chromatin silencing, genomic stability, and extended replicative lifespan. Loss of BNA6 would reduce NAD⁺ availability, impairing Sir2 function and shortening lifespan, consistent with a pro-longevity role for the gene's normal function.

Key pathways
de novo NAD+ biosynthesis (kynurenine pathway)Sir2/sirtuin NAD+-dependent deacetylase signalingcaloric restriction longevity pathway
Longevity influence
Pro-longevity
Lifespan effect
Decrease

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

Answer
Correct
Mechanism
Correct
Reasoning quality
5/5
Failure mode
Correct
Notes

The model correctly predicted pro_longevity for BNA6. The mechanistic reasoning is excellent and well-grounded: BNA6 encodes nicotinate-nucleotide diphosphorylase (carboxylating), which catalyzes a key step in de novo NAD+ biosynthesis via the kynurenine/tryptophan pathway. The model correctly connects NAD+ levels to Sir2/sirtuin activity and caloric restriction-induced longevity in yeast. The reasoning that loss of BNA6 would reduce NAD+ availability, impairing Sir2 function and shortening lifespan, is biochemically sound. The mechanism class of "deregulated_nutrient_sensing" is a reasonable categorization, though "metabolic" might be slightly more precise. Overall, this is a high-quality prediction with correct answer and sound mechanistic reasoning.

Raw API responses

solver

{
  "reasoning": "BNA6 encodes nicotinate-nucleotide diphosphorylase (carboxylating), which catalyzes the penultimate step in the de novo NAD⁺ biosynthesis pathway (the kynurenine/tryptophan pathway) in yeast, converting quinolinate to nicotinate mononucleotide (NaMN). NAD⁺ is a critical coenzyme and signaling molecule whose intracellular levels directly regulate the activity of Sir2/sirtuins, the yeast NAD⁺-dependent deacetylases that are central mediators of caloric restriction-induced longevity. By contributing to NAD⁺ biosynthesis, BNA6 supports sirtuin activity, which in turn promotes chromatin silencing, genomic stability, and extended replicative lifespan. Loss of BNA6 would reduce NAD⁺ availability, impairing Sir2 function and shortening lifespan, consistent with a pro-longevity role for the gene's normal function.",
  "confidence": 0.72,
  "key_pathways": [
    "de novo NAD+ biosynthesis (kynurenine pathway)",
    "Sir2/sirtuin NAD+-dependent deacetylase signaling",
    "caloric restriction longevity pathway"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for BNA6. The mechanistic reasoning is excellent and well-grounded: BNA6 encodes nicotinate-nucleotide diphosphorylase (carboxylating), which catalyzes a key step in de novo NAD+ biosynthesis via the kynurenine/tryptophan pathway. The model correctly connects NAD+ levels to Sir2/sirtuin activity and caloric restriction-induced longevity in yeast. The reasoning that loss of BNA6 would reduce NAD+ availability, impairing Sir2 function and shortening lifespan, is biochemically sound. The mechanism class of \"deregulated_nutrient_sensing\" is a reasonable categorization, though \"metabolic\" might be slightly more precise. Overall, this is a high-quality prediction with correct answer and sound mechanistic reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}