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ACS2

S. cerevisiae

acetate--CoA ligase ACS2

What the model saw

Gene: ACS2
Organism: Saccharomyces cerevisiae
Known functions: acetate--CoA ligase ACS2. AMP binding. acetyl-CoA synthetase activity. acid-ammonia (or amide) ligase activity.
View unredacted entry
acetate--CoA ligase ACS2. AMP binding. acetyl-CoA synthetase activity. acid-ammonia (or amide) ligase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
72%
Mechanism
Epigenetic alterations
Reasoning

ACS2 encodes the primary acetyl-CoA synthetase in S. cerevisiae that converts acetate to acetyl-CoA in the nucleus and cytoplasm. Nuclear acetyl-CoA is the obligate acetyl-donor for histone acetyltransferases (HATs), and ACS2-derived acetyl-CoA directly fuels histone H3 and H4 acetylation, maintaining transcriptionally active chromatin states. Loss of ACS2 reduces global histone acetylation, leading to epigenetic silencing of stress-response and metabolic genes. Because histone acetylation levels decline with age in yeast and maintenance of proper acetylation marks is associated with extended replicative lifespan, ACS2 activity supports pro-longevity epigenetic states. Additionally, acetyl-CoA availability links nutrient sensing (glucose metabolism) to chromatin regulation, placing ACS2 at a key node connecting metabolic status to aging-relevant gene expression programs.

Key pathways
Histone acetylation / chromatin remodeling (nuclear acetyl-CoA supply)Acetate-CoA metabolism (acetyl-CoA biosynthesis)Nutrient sensing-epigenome axis (glucose-acetyl-CoA-HAT signaling)
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 ACS2 in S. cerevisiae with high confidence (0.72). The mechanistic reasoning is excellent and well-supported by the literature: ACS2 is the primary nuclear/cytoplasmic acetyl-CoA synthetase, and its role in supplying acetyl-CoA for histone acetyltransferases (HATs) is well-established. The connection between ACS2-derived nuclear acetyl-CoA, histone acetylation maintenance, and replicative lifespan extension is accurate. The model correctly identifies the epigenetic mechanism as the primary pathway and appropriately links it to nutrient sensing. This is a high-quality, mechanistically sound prediction.

Raw API responses

solver

{
  "reasoning": "ACS2 encodes the primary acetyl-CoA synthetase in S. cerevisiae that converts acetate to acetyl-CoA in the nucleus and cytoplasm. Nuclear acetyl-CoA is the obligate acetyl-donor for histone acetyltransferases (HATs), and ACS2-derived acetyl-CoA directly fuels histone H3 and H4 acetylation, maintaining transcriptionally active chromatin states. Loss of ACS2 reduces global histone acetylation, leading to epigenetic silencing of stress-response and metabolic genes. Because histone acetylation levels decline with age in yeast and maintenance of proper acetylation marks is associated with extended replicative lifespan, ACS2 activity supports pro-longevity epigenetic states. Additionally, acetyl-CoA availability links nutrient sensing (glucose metabolism) to chromatin regulation, placing ACS2 at a key node connecting metabolic status to aging-relevant gene expression programs.",
  "confidence": 0.72,
  "key_pathways": [
    "Histone acetylation / chromatin remodeling (nuclear acetyl-CoA supply)",
    "Acetate-CoA metabolism (acetyl-CoA biosynthesis)",
    "Nutrient sensing-epigenome axis (glucose-acetyl-CoA-HAT signaling)"
  ],
  "mechanism_class": "epigenetic_alterations",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for ACS2 in S. cerevisiae with high confidence (0.72). The mechanistic reasoning is excellent and well-supported by the literature: ACS2 is the primary nuclear/cytoplasmic acetyl-CoA synthetase, and its role in supplying acetyl-CoA for histone acetyltransferases (HATs) is well-established. The connection between ACS2-derived nuclear acetyl-CoA, histone acetylation maintenance, and replicative lifespan extension is accurate. The model correctly identifies the epigenetic mechanism as the primary pathway and appropriately links it to nutrient sensing. This is a high-quality, mechanistically sound prediction.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}