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ACB1

S. cerevisiae

long-chain fatty acid transporter ACB1

What the model saw

Gene: ACB1
Organism: Saccharomyces cerevisiae
Known functions: long-chain fatty acid transporter ACB1. fatty-acyl-CoA binding. long-chain fatty acyl-CoA binding.
View unredacted entry
long-chain fatty acid transporter ACB1. fatty-acyl-CoA binding. long-chain fatty acyl-CoA binding.

Solver output

Predicted influence
Pro-longevity
Confidence
62%
Mechanism
Deregulated nutrient sensing
Reasoning

ACB1 encodes the acyl-CoA binding protein (ACBP) in S. cerevisiae, which binds long-chain fatty acyl-CoA esters with high affinity and facilitates their intracellular transport and sequestration. By buffering the free acyl-CoA pool, ACB1 regulates fatty acid metabolism, lipid biosynthesis, and membrane homeostasis. Proper acyl-CoA trafficking is essential for maintaining lipid homeostasis and mitochondrial function, both of which are critical determinants of yeast lifespan. Additionally, ACB1 has been implicated in autophagy induction under nutrient-limiting conditions — it is secreted unconventionally and acts as a pro-autophagic signal, linking lipid sensing to macroautophagy pathways that promote longevity. Loss of ACB1 disrupts acyl-CoA homeostasis and impairs autophagic flux, which is associated with shortened lifespan in yeast.

Key pathways
fatty acyl-CoA homeostasis and lipid metabolismnutrient sensing and lipid signalingautophagy induction via unconventional secretion
Longevity influence
Anti-longevity
Lifespan effect
Increase

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
Incorrect
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Confident wrong
Notes

The model predicted ACB1 as pro_longevity, but the ground truth is anti_longevity. The model's reasoning focused on ACB1's role in maintaining acyl-CoA homeostasis, lipid metabolism, and autophagy induction as beneficial for longevity. However, since ACB1 is actually anti-longevity (meaning its deletion or loss extends lifespan), the mechanistic reasoning is inverted. The model incorrectly concluded that loss of ACB1 shortens lifespan, when in fact deletion of ACB1 extends lifespan in yeast. The model showed moderate confidence (0.62) in the wrong direction. The reasoning about autophagy and acyl-CoA homeostasis may have some factual basis but was applied incorrectly to reach the wrong conclusion about longevity influence.

Raw API responses

solver

{
  "reasoning": "ACB1 encodes the acyl-CoA binding protein (ACBP) in S. cerevisiae, which binds long-chain fatty acyl-CoA esters with high affinity and facilitates their intracellular transport and sequestration. By buffering the free acyl-CoA pool, ACB1 regulates fatty acid metabolism, lipid biosynthesis, and membrane homeostasis. Proper acyl-CoA trafficking is essential for maintaining lipid homeostasis and mitochondrial function, both of which are critical determinants of yeast lifespan. Additionally, ACB1 has been implicated in autophagy induction under nutrient-limiting conditions — it is secreted unconventionally and acts as a pro-autophagic signal, linking lipid sensing to macroautophagy pathways that promote longevity. Loss of ACB1 disrupts acyl-CoA homeostasis and impairs autophagic flux, which is associated with shortened lifespan in yeast.",
  "confidence": 0.62,
  "key_pathways": [
    "fatty acyl-CoA homeostasis and lipid metabolism",
    "nutrient sensing and lipid signaling",
    "autophagy induction via unconventional secretion"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model predicted ACB1 as pro_longevity, but the ground truth is anti_longevity. The model's reasoning focused on ACB1's role in maintaining acyl-CoA homeostasis, lipid metabolism, and autophagy induction as beneficial for longevity. However, since ACB1 is actually anti-longevity (meaning its deletion or loss extends lifespan), the mechanistic reasoning is inverted. The model incorrectly concluded that loss of ACB1 shortens lifespan, when in fact deletion of ACB1 extends lifespan in yeast. The model showed moderate confidence (0.62) in the wrong direction. The reasoning about autophagy and acyl-CoA homeostasis may have some factual basis but was applied incorrectly to reach the wrong conclusion about longevity influence.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}
ACB1 · Saccharomyces cerevisiae | Aging biology eval