MIG1

S. cerevisiae

transcription factor MIG1

What the model saw

Gene: MIG1
Organism: Saccharomyces cerevisiae
Known functions: transcription factor MIG1. DNA-binding transcription repressor activity, RNA polymerase II-specific. RNA polymerase II cis-regulatory region sequence-specific DNA binding. protein binding. sequence-specific DNA binding. zinc ion binding.

View unredacted entry

transcription factor MIG1. DNA-binding transcription repressor activity, RNA polymerase II-specific. RNA polymerase II cis-regulatory region sequence-specific DNA binding. protein binding. sequence-specific DNA binding. zinc ion binding.

Solver output

Predicted influence

Anti-longevity

Confidence

78%

Mechanism

Deregulated nutrient sensing

Reasoning

MIG1 is a zinc-finger transcriptional repressor that mediates glucose repression in S. cerevisiae, acting downstream of the Snf1/AMPK pathway. Under high glucose conditions, MIG1 is active and represses genes involved in alternative carbon source utilization, gluconeogenesis, and respiration — including genes regulated by the Snf1 kinase pathway. This repression of metabolic flexibility and mitochondrial respiration mimics a nutrient-sensing state that opposes longevity. Snf1/AMPK activation (which inactivates MIG1) is a well-established pro-longevity signal in yeast, analogous to AMPK activation in higher eukaryotes. Therefore, MIG1's normal function as a glucose-responsive repressor promotes a high-nutrient signaling state that shortens lifespan, placing it in opposition to longevity.

Key pathways

glucose repression / Snf1-AMPK signalingcarbon catabolite repressionnutrient sensing and metabolic flexibility

Longevity influence

Anti-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 MIG1 as anti_longevity with high confidence (0.78). The mechanistic reasoning is excellent: MIG1 is accurately described as a zinc-finger transcriptional repressor mediating glucose repression downstream of Snf1/AMPK. The model correctly identifies that MIG1 represses metabolic flexibility and respiration under high glucose, and that Snf1 activation (which inactivates MIG1) is pro-longevity. The connection to nutrient sensing and the analogy to AMPK signaling in higher eukaryotes is well-reasoned and accurate. The mechanism class "deregulated_nutrient_sensing" is appropriate.

Raw API responses

solver

{
  "reasoning": "MIG1 is a zinc-finger transcriptional repressor that mediates glucose repression in S. cerevisiae, acting downstream of the Snf1/AMPK pathway. Under high glucose conditions, MIG1 is active and represses genes involved in alternative carbon source utilization, gluconeogenesis, and respiration — including genes regulated by the Snf1 kinase pathway. This repression of metabolic flexibility and mitochondrial respiration mimics a nutrient-sensing state that opposes longevity. Snf1/AMPK activation (which inactivates MIG1) is a well-established pro-longevity signal in yeast, analogous to AMPK activation in higher eukaryotes. Therefore, MIG1's normal function as a glucose-responsive repressor promotes a high-nutrient signaling state that shortens lifespan, placing it in opposition to longevity.",
  "confidence": 0.78,
  "key_pathways": [
    "glucose repression / Snf1-AMPK signaling",
    "carbon catabolite repression",
    "nutrient sensing and metabolic flexibility"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted MIG1 as anti_longevity with high confidence (0.78). The mechanistic reasoning is excellent: MIG1 is accurately described as a zinc-finger transcriptional repressor mediating glucose repression downstream of Snf1/AMPK. The model correctly identifies that MIG1 represses metabolic flexibility and respiration under high glucose, and that Snf1 activation (which inactivates MIG1) is pro-longevity. The connection to nutrient sensing and the analogy to AMPK signaling in higher eukaryotes is well-reasoned and accurate. The mechanism class \"deregulated_nutrient_sensing\" is appropriate.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}