BIR1
S. cerevisiae
survivin
What the model saw
Gene: BIR1 Organism: Saccharomyces cerevisiae Known functions: survivin. protein binding. zinc ion binding.
View unredacted entry
survivin. protein binding. zinc ion binding.
Solver output
BIR1 is the yeast homolog of survivin, a member of the inhibitor of apoptosis (IAP) protein family that contains a BIR (Baculoviral IAP Repeat) domain. Survivin functions as a chromosomal passenger complex (CPC) component critical for proper chromosome segregation during mitosis and cytokinesis. In yeast, BIR1 participates in the CPC alongside Sli15/INCENP and Ipl1/Aurora B kinase, regulating spindle assembly checkpoint and ensuring accurate chromosome segregation. Errors in chromosome segregation driven by CPC dysregulation contribute to genomic instability and aneuploidy, which are hallmarks associated with cellular aging. Additionally, survivin/BIR1's role in suppressing apoptosis-like cell death pathways in yeast means its normal function may promote survival of damaged or aneuploid cells, potentially accelerating replicative aging rather than extending lifespan. Zinc ion binding supports the structural integrity of the BIR domain required for these protein–protein interactions within the CPC.
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 anti_longevity but the ground truth is pro_longevity. The model correctly identified BIR1 as the yeast survivin homolog and its role in the Chromosomal Passenger Complex (CPC), but then incorrectly reasoned that its function would be anti-longevity. The model's logic that survivin/BIR1 "promotes survival of damaged or aneuploid cells, potentially accelerating replicative aging" is speculative and contradicts the actual finding. In reality, BIR1 as a pro-longevity gene likely means its proper function (ensuring accurate chromosome segregation, maintaining genomic stability) extends lifespan, and loss of BIR1 would shorten lifespan. The model's mechanistic reasoning about IAP/apoptosis suppression accelerating aging is not well-supported and led to the wrong conclusion. Confidence was 0.62, which is moderately confident in the wrong direction.
Raw API responses
solver
{
"reasoning": "BIR1 is the yeast homolog of survivin, a member of the inhibitor of apoptosis (IAP) protein family that contains a BIR (Baculoviral IAP Repeat) domain. Survivin functions as a chromosomal passenger complex (CPC) component critical for proper chromosome segregation during mitosis and cytokinesis. In yeast, BIR1 participates in the CPC alongside Sli15/INCENP and Ipl1/Aurora B kinase, regulating spindle assembly checkpoint and ensuring accurate chromosome segregation. Errors in chromosome segregation driven by CPC dysregulation contribute to genomic instability and aneuploidy, which are hallmarks associated with cellular aging. Additionally, survivin/BIR1's role in suppressing apoptosis-like cell death pathways in yeast means its normal function may promote survival of damaged or aneuploid cells, potentially accelerating replicative aging rather than extending lifespan. Zinc ion binding supports the structural integrity of the BIR domain required for these protein–protein interactions within the CPC.",
"confidence": 0.62,
"key_pathways": [
"Chromosomal Passenger Complex (CPC) / spindle assembly checkpoint",
"Ipl1/Aurora B kinase signaling",
"Inhibitor of apoptosis (IAP) / cell death suppression"
],
"mechanism_class": "cellular_senescence",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model predicted anti_longevity but the ground truth is pro_longevity. The model correctly identified BIR1 as the yeast survivin homolog and its role in the Chromosomal Passenger Complex (CPC), but then incorrectly reasoned that its function would be anti-longevity. The model's logic that survivin/BIR1 \"promotes survival of damaged or aneuploid cells, potentially accelerating replicative aging\" is speculative and contradicts the actual finding. In reality, BIR1 as a pro-longevity gene likely means its proper function (ensuring accurate chromosome segregation, maintaining genomic stability) extends lifespan, and loss of BIR1 would shorten lifespan. The model's mechanistic reasoning about IAP/apoptosis suppression accelerating aging is not well-supported and led to the wrong conclusion. Confidence was 0.62, which is moderately confident in the wrong direction.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}