MsrA
D. melanogaster
Methionine sulfoxide reductase A
What the model saw
Gene: MsrA Organism: Drosophila melanogaster Known functions: Methionine sulfoxide reductase A. methionine sulfoxide reductase A. L-methionine (S)-S-oxide reductase activity. peptide-methionine (S)-S-oxide reductase activity.
View unredacted entry
Methionine sulfoxide reductase A. methionine sulfoxide reductase A. L-methionine (S)-S-oxide reductase activity. peptide-methionine (S)-S-oxide reductase activity.
Solver output
MsrA encodes Methionine Sulfoxide Reductase A, which catalyzes the stereospecific reduction of the (S)-epimer of oxidized methionine residues (methionine sulfoxide) back to methionine, both in free amino acids and within peptides/proteins. This repair activity directly counteracts oxidative damage to proteins, restoring their structure and function. By reversing methionine oxidation — a key form of reactive oxygen species (ROS)-induced protein damage — MsrA maintains proteostasis and reduces the accumulation of oxidatively damaged proteins that would otherwise impair cellular function. Overexpression of MsrA has been shown in multiple organisms, including Drosophila, to extend lifespan, while loss of function accelerates aging phenotypes. This places MsrA squarely in the antioxidant/protein repair axis that opposes age-related proteostasis decline.
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
The model correctly predicted pro_longevity with high confidence (0.92). The mechanistic reasoning is accurate and detailed: MsrA reduces oxidized methionine residues, counteracting oxidative protein damage, maintaining proteostasis, and extending lifespan when overexpressed in Drosophila. The model correctly references both overexpression extending lifespan and loss-of-function accelerating aging. The mechanism classification as "loss_of_proteostasis" is appropriate since MsrA prevents proteostasis decline. All aspects of the prediction are correct and well-reasoned.
Raw API responses
solver
{
"reasoning": "MsrA encodes Methionine Sulfoxide Reductase A, which catalyzes the stereospecific reduction of the (S)-epimer of oxidized methionine residues (methionine sulfoxide) back to methionine, both in free amino acids and within peptides/proteins. This repair activity directly counteracts oxidative damage to proteins, restoring their structure and function. By reversing methionine oxidation — a key form of reactive oxygen species (ROS)-induced protein damage — MsrA maintains proteostasis and reduces the accumulation of oxidatively damaged proteins that would otherwise impair cellular function. Overexpression of MsrA has been shown in multiple organisms, including Drosophila, to extend lifespan, while loss of function accelerates aging phenotypes. This places MsrA squarely in the antioxidant/protein repair axis that opposes age-related proteostasis decline.",
"confidence": 0.92,
"key_pathways": [
"methionine sulfoxide reduction / protein oxidative repair",
"reactive oxygen species (ROS) detoxification",
"proteostasis maintenance"
],
"mechanism_class": "loss_of_proteostasis",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity with high confidence (0.92). The mechanistic reasoning is accurate and detailed: MsrA reduces oxidized methionine residues, counteracting oxidative protein damage, maintaining proteostasis, and extending lifespan when overexpressed in Drosophila. The model correctly references both overexpression extending lifespan and loss-of-function accelerating aging. The mechanism classification as \"loss_of_proteostasis\" is appropriate since MsrA prevents proteostasis decline. All aspects of the prediction are correct and well-reasoned.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}