FCY1
S. cerevisiae
cytosine deaminase
What the model saw
Gene: FCY1 Organism: Saccharomyces cerevisiae Known functions: cytosine deaminase. cytosine deaminase activity. diaminohydroxyphosphoribosylaminopyrimidine deaminase activity. hydrolase activity. zinc ion binding.
View unredacted entry
cytosine deaminase. cytosine deaminase activity. diaminohydroxyphosphoribosylaminopyrimidine deaminase activity. hydrolase activity. zinc ion binding.
Solver output
FCY1 encodes cytosine deaminase, a zinc-dependent hydrolase that converts cytosine to uracil in the pyrimidine salvage pathway. This enzyme is primarily involved in nucleobase recycling and is not directly linked to canonical aging hallmark pathways such as nutrient sensing, proteostasis, or genomic maintenance. While nucleotide pool imbalances can theoretically contribute to genomic instability, cytosine deaminase activity in yeast operates on exogenous cytosine salvage rather than on DNA/RNA directly, making a direct pro- or anti-longevity assignment difficult. The diaminohydroxyphosphoribosylaminopyrimidine deaminase activity also points to a secondary role in folate/riboflavin biosynthesis-adjacent metabolism, which could modestly influence one-carbon metabolism but without strong evidence linking FCY1 specifically to lifespan regulation. No robust genetic evidence in yeast lifespan screens strongly implicates FCY1 in either replicative or chronological longevity.
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 predicted "unclear" with moderate confidence (0.42), but the ground truth is "anti_longevity." The model's reasoning focused on pyrimidine salvage and nucleotide metabolism, concluding there was insufficient evidence to make a determination. FCY1 is classified as anti-longevity in GenAge, meaning its deletion extends lifespan. The model failed to identify this relationship and instead hedged inappropriately. The mechanistic reasoning about cytosine deaminase and pyrimidine salvage is technically accurate for the gene's known function, but the model did not connect this to any longevity mechanism. The model's claim that "no robust genetic evidence in yeast lifespan screens strongly implicates FCY1" appears to be incorrect given the GenAge classification. The reasoning quality is low because the model essentially gave up without making a correct prediction.
Raw API responses
solver
{
"reasoning": "FCY1 encodes cytosine deaminase, a zinc-dependent hydrolase that converts cytosine to uracil in the pyrimidine salvage pathway. This enzyme is primarily involved in nucleobase recycling and is not directly linked to canonical aging hallmark pathways such as nutrient sensing, proteostasis, or genomic maintenance. While nucleotide pool imbalances can theoretically contribute to genomic instability, cytosine deaminase activity in yeast operates on exogenous cytosine salvage rather than on DNA/RNA directly, making a direct pro- or anti-longevity assignment difficult. The diaminohydroxyphosphoribosylaminopyrimidine deaminase activity also points to a secondary role in folate/riboflavin biosynthesis-adjacent metabolism, which could modestly influence one-carbon metabolism but without strong evidence linking FCY1 specifically to lifespan regulation. No robust genetic evidence in yeast lifespan screens strongly implicates FCY1 in either replicative or chronological longevity.",
"confidence": 0.42,
"key_pathways": [
"pyrimidine salvage pathway",
"nucleotide metabolism",
"zinc-dependent hydrolase activity"
],
"mechanism_class": "other",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" with moderate confidence (0.42), but the ground truth is \"anti_longevity.\" The model's reasoning focused on pyrimidine salvage and nucleotide metabolism, concluding there was insufficient evidence to make a determination. FCY1 is classified as anti-longevity in GenAge, meaning its deletion extends lifespan. The model failed to identify this relationship and instead hedged inappropriately. The mechanistic reasoning about cytosine deaminase and pyrimidine salvage is technically accurate for the gene's known function, but the model did not connect this to any longevity mechanism. The model's claim that \"no robust genetic evidence in yeast lifespan screens strongly implicates FCY1\" appears to be incorrect given the GenAge classification. The reasoning quality is low because the model essentially gave up without making a correct prediction.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}