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MXR1

S. cerevisiae

peptide-methionine-S-sulfoxide reductase

What the model saw

Gene: MXR1
Organism: Saccharomyces cerevisiae
Known functions: peptide-methionine-S-sulfoxide reductase. L-methionine (S)-S-oxide reductase activity. peptide-methionine (S)-S-oxide reductase activity.
View unredacted entry
peptide-methionine-S-sulfoxide reductase. L-methionine (S)-S-oxide reductase activity. peptide-methionine (S)-S-oxide reductase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
88%
Mechanism
Loss of proteostasis
Reasoning

MXR1 encodes peptide-methionine-(S)-S-oxide reductase (MsrA), which catalyzes the reduction of oxidized methionine residues (methionine sulfoxide) back to methionine in proteins. This repair activity is a critical component of the cellular defense against oxidative protein damage. By reversing methionine oxidation, MXR1 restores the structural and functional integrity of oxidatively damaged proteins, directly supporting proteostasis. In yeast, overexpression of MsrA has been shown to extend replicative and chronological lifespan, while deletion shortens it, consistent with a pro-longevity role. The methionine sulfoxide reductase system also acts as a catalytic antioxidant by scavenging reactive oxygen species through cyclic oxidation/reduction of surface-exposed methionines, further reducing oxidative stress burden during aging.

Key pathways
methionine sulfoxide reduction / oxidative protein repairreactive oxygen species scavenging via methionine cyclingproteostasis maintenance under oxidative stress
Longevity influence
Pro-longevity
Lifespan effect
Increase and 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 MXR1 in S. cerevisiae with high confidence (0.88). The mechanistic reasoning is excellent and accurate: MXR1 encodes methionine sulfoxide reductase A (MsrA), which repairs oxidized methionine residues in proteins, supporting proteostasis and reducing oxidative stress. The model correctly notes that overexpression extends lifespan while deletion shortens it. The ROS scavenging via methionine cycling mechanism is also well-described. All aspects of the prediction are accurate and well-supported.

Raw API responses

solver

{
  "reasoning": "MXR1 encodes peptide-methionine-(S)-S-oxide reductase (MsrA), which catalyzes the reduction of oxidized methionine residues (methionine sulfoxide) back to methionine in proteins. This repair activity is a critical component of the cellular defense against oxidative protein damage. By reversing methionine oxidation, MXR1 restores the structural and functional integrity of oxidatively damaged proteins, directly supporting proteostasis. In yeast, overexpression of MsrA has been shown to extend replicative and chronological lifespan, while deletion shortens it, consistent with a pro-longevity role. The methionine sulfoxide reductase system also acts as a catalytic antioxidant by scavenging reactive oxygen species through cyclic oxidation/reduction of surface-exposed methionines, further reducing oxidative stress burden during aging.",
  "confidence": 0.88,
  "key_pathways": [
    "methionine sulfoxide reduction / oxidative protein repair",
    "reactive oxygen species scavenging via methionine cycling",
    "proteostasis maintenance under oxidative stress"
  ],
  "mechanism_class": "loss_of_proteostasis",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for MXR1 in S. cerevisiae with high confidence (0.88). The mechanistic reasoning is excellent and accurate: MXR1 encodes methionine sulfoxide reductase A (MsrA), which repairs oxidized methionine residues in proteins, supporting proteostasis and reducing oxidative stress. The model correctly notes that overexpression extends lifespan while deletion shortens it. The ROS scavenging via methionine cycling mechanism is also well-described. All aspects of the prediction are accurate and well-supported.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}