cdc-25.1
C. elegans
M-phase inducer phosphatase cdc-25.1
What the model saw
Gene: cdc-25.1 Organism: Caenorhabditis elegans Known functions: M-phase inducer phosphatase cdc-25.1. phosphoprotein phosphatase activity. protein binding. protein tyrosine phosphatase activity.
View unredacted entry
M-phase inducer phosphatase cdc-25.1. phosphoprotein phosphatase activity. protein binding. protein tyrosine phosphatase activity.
Solver output
CDC-25.1 is an M-phase inducer phosphatase (a CDC25 family dual-specificity phosphatase) that activates cyclin-dependent kinases (CDKs) by removing inhibitory phosphorylations on tyrosine and threonine residues, thereby driving cell cycle progression into mitosis. Promoting cell cycle entry and proliferation, particularly in stem/progenitor compartments, is generally associated with increased replicative stress, genomic instability, and accelerated tissue aging rather than longevity. In C. elegans, enhanced CDC-25.1 activity has been linked to increased germline proliferation; notably, reduced germline proliferation (e.g., via germline ablation) is a well-established pro-longevity intervention in this organism. By sustaining mitotic entry and proliferative signaling, cdc-25.1 opposes the longevity benefit conferred by germline stem cell quiescence, acting through the DAF-16/FOXO and lipid metabolism axis downstream of germline signals. Its phosphatase activity on CDK inhibitory sites thus functionally antagonizes longevity pathways tied to stem cell and proliferation control.
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 anti_longevity for cdc-25.1 in C. elegans. The mechanistic reasoning is sound: CDC-25.1 promotes cell cycle progression and germline proliferation, and increased germline proliferation is known to be anti-longevity in C. elegans (germline ablation extends lifespan via DAF-16/FOXO). The model correctly identifies the CDK activation pathway and the germline proliferation/DAF-16 axis. The mechanism_class of "cellular_senescence" is a slight mismatch — the mechanism is more about germline proliferation signaling than cellular senescence per se — but the overall reasoning is well-grounded. Confidence of 0.72 is appropriate.
Raw API responses
solver
{
"reasoning": "CDC-25.1 is an M-phase inducer phosphatase (a CDC25 family dual-specificity phosphatase) that activates cyclin-dependent kinases (CDKs) by removing inhibitory phosphorylations on tyrosine and threonine residues, thereby driving cell cycle progression into mitosis. Promoting cell cycle entry and proliferation, particularly in stem/progenitor compartments, is generally associated with increased replicative stress, genomic instability, and accelerated tissue aging rather than longevity. In C. elegans, enhanced CDC-25.1 activity has been linked to increased germline proliferation; notably, reduced germline proliferation (e.g., via germline ablation) is a well-established pro-longevity intervention in this organism. By sustaining mitotic entry and proliferative signaling, cdc-25.1 opposes the longevity benefit conferred by germline stem cell quiescence, acting through the DAF-16/FOXO and lipid metabolism axis downstream of germline signals. Its phosphatase activity on CDK inhibitory sites thus functionally antagonizes longevity pathways tied to stem cell and proliferation control.",
"confidence": 0.72,
"key_pathways": [
"CDK activation / cell cycle G2-M transition",
"germline proliferation signaling (DAF-16/FOXO axis)",
"replicative stress and genomic instability"
],
"mechanism_class": "cellular_senescence",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for cdc-25.1 in C. elegans. The mechanistic reasoning is sound: CDC-25.1 promotes cell cycle progression and germline proliferation, and increased germline proliferation is known to be anti-longevity in C. elegans (germline ablation extends lifespan via DAF-16/FOXO). The model correctly identifies the CDK activation pathway and the germline proliferation/DAF-16 axis. The mechanism_class of \"cellular_senescence\" is a slight mismatch — the mechanism is more about germline proliferation signaling than cellular senescence per se — but the overall reasoning is well-grounded. Confidence of 0.72 is appropriate.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}