TSA1
S. cerevisiae
thioredoxin peroxidase TSA1
What the model saw
Gene: TSA1 Organism: Saccharomyces cerevisiae Known functions: thioredoxin peroxidase TSA1. antioxidant activity. identical protein binding. kinase regulator activity. oxidoreductase activity. peroxiredoxin activity. protein binding. ribosome binding. thioredoxin peroxidase activity. thioredoxin-dependent peroxiredoxin activity. unfolded protein binding.
View unredacted entry
thioredoxin peroxidase TSA1. antioxidant activity. identical protein binding. kinase regulator activity. oxidoreductase activity. peroxiredoxin activity. protein binding. ribosome binding. thioredoxin peroxidase activity. thioredoxin-dependent peroxiredoxin activity. unfolded protein binding.
Solver output
TSA1 encodes the major cytoplasmic thioredoxin peroxidase (peroxiredoxin) in S. cerevisiae, which uses thioredoxin as an electron donor to reduce and detoxify hydrogen peroxide and other reactive oxygen species (ROS). By scavenging ROS, TSA1 directly limits oxidative damage to proteins, lipids, and DNA, thereby opposing a key driver of cellular aging. Its thioredoxin-dependent peroxiredoxin activity places it centrally in the thioredoxin antioxidant pathway, and loss of TSA1 is well-documented to shorten both replicative and chronological lifespan in yeast. Additionally, its unfolded protein binding and ribosome-binding activities suggest a chaperone-like role in maintaining proteostasis under oxidative stress, further supporting longevity. The kinase regulator activity may also link TSA1 to stress-response signaling (e.g., modulation of Hog1/MAPK), reinforcing its pro-survival function.
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 predicts TSA1 as pro_longevity with high confidence (0.93), which matches the ground truth. The core mechanistic reasoning is largely correct — TSA1 is indeed a thioredoxin peroxidase that scavenges ROS and its loss shortens lifespan in yeast. However, the model incorrectly classifies the mechanism_class as "mitochondrial_dysfunction," which is inaccurate. TSA1 is a cytoplasmic peroxiredoxin acting primarily through the thioredoxin antioxidant pathway and oxidative stress defense — not through mitochondrial dysfunction. The primary mechanism should be classified as oxidative stress resistance or antioxidant defense. The reasoning text itself is mostly accurate and well-articulated, but the mechanism_class label is a notable error.
Raw API responses
solver
{
"reasoning": "TSA1 encodes the major cytoplasmic thioredoxin peroxidase (peroxiredoxin) in S. cerevisiae, which uses thioredoxin as an electron donor to reduce and detoxify hydrogen peroxide and other reactive oxygen species (ROS). By scavenging ROS, TSA1 directly limits oxidative damage to proteins, lipids, and DNA, thereby opposing a key driver of cellular aging. Its thioredoxin-dependent peroxiredoxin activity places it centrally in the thioredoxin antioxidant pathway, and loss of TSA1 is well-documented to shorten both replicative and chronological lifespan in yeast. Additionally, its unfolded protein binding and ribosome-binding activities suggest a chaperone-like role in maintaining proteostasis under oxidative stress, further supporting longevity. The kinase regulator activity may also link TSA1 to stress-response signaling (e.g., modulation of Hog1/MAPK), reinforcing its pro-survival function.",
"confidence": 0.93,
"key_pathways": [
"Thioredoxin/peroxiredoxin antioxidant pathway",
"Reactive oxygen species (ROS) detoxification",
"Oxidative stress response signaling (Hog1/MAPK)"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicts TSA1 as pro_longevity with high confidence (0.93), which matches the ground truth. The core mechanistic reasoning is largely correct — TSA1 is indeed a thioredoxin peroxidase that scavenges ROS and its loss shortens lifespan in yeast. However, the model incorrectly classifies the mechanism_class as \"mitochondrial_dysfunction,\" which is inaccurate. TSA1 is a cytoplasmic peroxiredoxin acting primarily through the thioredoxin antioxidant pathway and oxidative stress defense — not through mitochondrial dysfunction. The primary mechanism should be classified as oxidative stress resistance or antioxidant defense. The reasoning text itself is mostly accurate and well-articulated, but the mechanism_class label is a notable error.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": true,
"mechanism_correct": false,
"reasoning_quality": 4,
"ground_truth_questionable": false
}