YOR1
S. cerevisiae
ATP-binding cassette transporter YOR1
What the model saw
Gene: YOR1 Organism: Saccharomyces cerevisiae Known functions: ATP-binding cassette transporter YOR1. ABC-type cadmium transporter activity. ABC-type glutathione S-conjugate transporter activity. ABC-type transporter activity. ABC-type xenobiotic transporter activity. ATP binding. ATP hydrolysis activity. protein binding.
View unredacted entry
ATP-binding cassette transporter YOR1. ABC-type cadmium transporter activity. ABC-type glutathione S-conjugate transporter activity. ABC-type transporter activity. ABC-type xenobiotic transporter activity. ATP binding. ATP hydrolysis activity. protein binding.
Solver output
YOR1 encodes an ABC transporter in the plasma membrane of S. cerevisiae that uses ATP hydrolysis to actively export xenobiotics, cadmium ions, and glutathione S-conjugates out of the cell. By expelling toxic heavy metals (cadmium) and electrophilic glutathione conjugates—byproducts of oxidative and xenobiotic stress—YOR1 reduces intracellular accumulation of cytotoxic compounds that would otherwise damage proteins, lipids, and nucleic acids. This detoxification function directly opposes oxidative damage and proteotoxic stress, both of which are drivers of cellular aging. Loss of YOR1 in yeast leads to hypersensitivity to oxidants and heavy metals, consistent with accelerated cellular damage. The glutathione S-conjugate export activity also links YOR1 to maintenance of the glutathione redox pool, supporting antioxidant capacity and proteostasis.
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 for YOR1 with a reasonable confidence of 0.72. The mechanistic reasoning is sound and well-grounded: YOR1 as an ABC transporter exports toxic compounds (cadmium, glutathione S-conjugates, xenobiotics), reducing intracellular cytotoxic burden and oxidative stress, which supports longevity. The connection to glutathione redox homeostasis and oxidative stress resistance is appropriate. The reasoning is coherent and biologically plausible, though it could be noted that the specific experimental evidence for YOR1's role in replicative or chronological lifespan extension in yeast wasn't explicitly cited (e.g., deletion studies showing shortened lifespan). Overall, a strong and well-reasoned prediction.
Raw API responses
solver
{
"reasoning": "YOR1 encodes an ABC transporter in the plasma membrane of S. cerevisiae that uses ATP hydrolysis to actively export xenobiotics, cadmium ions, and glutathione S-conjugates out of the cell. By expelling toxic heavy metals (cadmium) and electrophilic glutathione conjugates—byproducts of oxidative and xenobiotic stress—YOR1 reduces intracellular accumulation of cytotoxic compounds that would otherwise damage proteins, lipids, and nucleic acids. This detoxification function directly opposes oxidative damage and proteotoxic stress, both of which are drivers of cellular aging. Loss of YOR1 in yeast leads to hypersensitivity to oxidants and heavy metals, consistent with accelerated cellular damage. The glutathione S-conjugate export activity also links YOR1 to maintenance of the glutathione redox pool, supporting antioxidant capacity and proteostasis.",
"confidence": 0.72,
"key_pathways": [
"ABC transporter-mediated xenobiotic/heavy metal detoxification",
"glutathione S-conjugate export and redox homeostasis",
"oxidative stress resistance"
],
"mechanism_class": "other",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for YOR1 with a reasonable confidence of 0.72. The mechanistic reasoning is sound and well-grounded: YOR1 as an ABC transporter exports toxic compounds (cadmium, glutathione S-conjugates, xenobiotics), reducing intracellular cytotoxic burden and oxidative stress, which supports longevity. The connection to glutathione redox homeostasis and oxidative stress resistance is appropriate. The reasoning is coherent and biologically plausible, though it could be noted that the specific experimental evidence for YOR1's role in replicative or chronological lifespan extension in yeast wasn't explicitly cited (e.g., deletion studies showing shortened lifespan). Overall, a strong and well-reasoned prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}