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TAT2

S. cerevisiae

aromatic amino acid transmembrane transporter TAT2

What the model saw

Gene: TAT2
Organism: Saccharomyces cerevisiae
Known functions: aromatic amino acid transmembrane transporter TAT2. amino acid transmembrane transporter activity. aromatic amino acid transmembrane transporter activity. catalytic activity. high-affinity tryptophan transmembrane transporter activity.
View unredacted entry
aromatic amino acid transmembrane transporter TAT2. amino acid transmembrane transporter activity. aromatic amino acid transmembrane transporter activity. catalytic activity. high-affinity tryptophan transmembrane transporter activity.

Solver output

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

TAT2 is the high-affinity tryptophan permease in S. cerevisiae, responsible for importing tryptophan and other aromatic amino acids across the plasma membrane. Elevated intracellular tryptophan levels, driven by TAT2 activity, feed into the TOR (Target of Rapamycin) signaling pathway by sustaining amino acid sufficiency signals that activate TORC1. TORC1 activation suppresses autophagy and stress-response programs that are pro-longevity. Consistent with this, TAT2 overexpression has been shown to shorten chronological lifespan in yeast, while its degradation (e.g., under rapamycin treatment or nutrient limitation) is associated with lifespan extension. Thus, the normal pro-transport function of TAT2 promotes TORC1 activity and opposes longevity.

Key pathways
TOR/TORC1 nutrient sensingtryptophan import and amino acid availabilityautophagy suppression via TORC1
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
Correct
Mechanism
Correct
Reasoning quality
5/5
Failure mode
Correct
Notes

The model correctly predicted TAT2 as anti_longevity with high confidence (0.72). The mechanistic reasoning is detailed and accurate: TAT2 is indeed the high-affinity tryptophan permease, and its activity sustains amino acid sufficiency signals that activate TORC1, which suppresses pro-longevity autophagy and stress-response programs. The model correctly notes that TAT2 overexpression shortens chronological lifespan and that its degradation (e.g., under rapamycin) is associated with lifespan extension. The key pathways identified (TOR/TORC1 nutrient sensing, tryptophan import, autophagy suppression) are all relevant and correct.

Raw API responses

solver

{
  "reasoning": "TAT2 is the high-affinity tryptophan permease in S. cerevisiae, responsible for importing tryptophan and other aromatic amino acids across the plasma membrane. Elevated intracellular tryptophan levels, driven by TAT2 activity, feed into the TOR (Target of Rapamycin) signaling pathway by sustaining amino acid sufficiency signals that activate TORC1. TORC1 activation suppresses autophagy and stress-response programs that are pro-longevity. Consistent with this, TAT2 overexpression has been shown to shorten chronological lifespan in yeast, while its degradation (e.g., under rapamycin treatment or nutrient limitation) is associated with lifespan extension. Thus, the normal pro-transport function of TAT2 promotes TORC1 activity and opposes longevity.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR/TORC1 nutrient sensing",
    "tryptophan import and amino acid availability",
    "autophagy suppression via TORC1"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted TAT2 as anti_longevity with high confidence (0.72). The mechanistic reasoning is detailed and accurate: TAT2 is indeed the high-affinity tryptophan permease, and its activity sustains amino acid sufficiency signals that activate TORC1, which suppresses pro-longevity autophagy and stress-response programs. The model correctly notes that TAT2 overexpression shortens chronological lifespan and that its degradation (e.g., under rapamycin) is associated with lifespan extension. The key pathways identified (TOR/TORC1 nutrient sensing, tryptophan import, autophagy suppression) are all relevant and correct.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}