CDC13
S. cerevisiae
telomere-binding protein CDC13
What the model saw
Gene: CDC13 Organism: Saccharomyces cerevisiae Known functions: telomere-binding protein CDC13. DNA binding. G-rich strand telomeric DNA binding. identical protein binding. protein binding. single-stranded telomeric DNA binding. telomerase inhibitor activity. translation elongation factor binding.
View unredacted entry
telomere-binding protein CDC13. DNA binding. G-rich strand telomeric DNA binding. identical protein binding. protein binding. single-stranded telomeric DNA binding. telomerase inhibitor activity. translation elongation factor binding.
Solver output
CDC13 is a single-stranded G-rich telomeric DNA-binding protein that forms the CST (Cdc13-Stn1-Ten1) complex, which is essential for telomere end protection in S. cerevisiae. By capping the single-stranded 3' overhang of telomeres, CDC13 prevents telomere degradation, inappropriate DNA damage checkpoint activation, and end-to-end chromosome fusions — all hallmarks of telomere attrition. Loss of CDC13 leads to extensive telomeric ssDNA accumulation, checkpoint-mediated growth arrest, and premature cellular senescence. Although CDC13 also has telomerase inhibitor activity (recruiting the Stn1-Ten1 module to limit telomerase access after elongation), this is part of a regulated fill-in mechanism that maintains telomere length homeostasis rather than causing net shortening. The dominant function — protecting telomere integrity — is pro-longevity, as cells lacking CDC13 undergo rapid replicative senescence.
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 CDC13 as pro_longevity with high confidence (0.82). The mechanistic reasoning is excellent and accurate: CDC13 functions as part of the CST complex to protect telomere ends, prevent ssDNA accumulation, suppress inappropriate DNA damage checkpoint activation, and maintain telomere integrity. The model correctly notes that loss of CDC13 leads to replicative senescence, making it pro-longevity. The model also correctly addresses the apparent paradox of CDC13's telomerase inhibitor activity, explaining it as part of regulated telomere length homeostasis rather than net shortening. The reasoning is thorough, mechanistically sound, and well-supported by the known biology of CDC13 in S. cerevisiae.
Raw API responses
solver
{
"reasoning": "CDC13 is a single-stranded G-rich telomeric DNA-binding protein that forms the CST (Cdc13-Stn1-Ten1) complex, which is essential for telomere end protection in S. cerevisiae. By capping the single-stranded 3' overhang of telomeres, CDC13 prevents telomere degradation, inappropriate DNA damage checkpoint activation, and end-to-end chromosome fusions — all hallmarks of telomere attrition. Loss of CDC13 leads to extensive telomeric ssDNA accumulation, checkpoint-mediated growth arrest, and premature cellular senescence. Although CDC13 also has telomerase inhibitor activity (recruiting the Stn1-Ten1 module to limit telomerase access after elongation), this is part of a regulated fill-in mechanism that maintains telomere length homeostasis rather than causing net shortening. The dominant function — protecting telomere integrity — is pro-longevity, as cells lacking CDC13 undergo rapid replicative senescence.",
"confidence": 0.82,
"key_pathways": [
"CST complex-mediated telomere capping",
"telomere length homeostasis / telomerase regulation",
"DNA damage checkpoint suppression at telomeres"
],
"mechanism_class": "telomere_attrition",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted CDC13 as pro_longevity with high confidence (0.82). The mechanistic reasoning is excellent and accurate: CDC13 functions as part of the CST complex to protect telomere ends, prevent ssDNA accumulation, suppress inappropriate DNA damage checkpoint activation, and maintain telomere integrity. The model correctly notes that loss of CDC13 leads to replicative senescence, making it pro-longevity. The model also correctly addresses the apparent paradox of CDC13's telomerase inhibitor activity, explaining it as part of regulated telomere length homeostasis rather than net shortening. The reasoning is thorough, mechanistically sound, and well-supported by the known biology of CDC13 in S. cerevisiae.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}