PCL7
S. cerevisiae
Pcl7p
What the model saw
Gene: PCL7 Organism: Saccharomyces cerevisiae Known functions: Pcl7p. cyclin-dependent protein serine/threonine kinase regulator activity. protein binding. protein kinase binding.
View unredacted entry
Pcl7p. cyclin-dependent protein serine/threonine kinase regulator activity. protein binding. protein kinase binding.
Solver output
PCL7 encodes a Pho85-associated cyclin (Pcl7p) in S. cerevisiae that acts as a regulatory subunit for cyclin-dependent kinases (CDKs), specifically Pho85. Pho85 cyclins modulate nutrient-sensing pathways, including phosphate sensing and connections to the TOR/PKA nutrient-sensing network. By activating Pho85-CDK complexes, PCL7 promotes cell cycle progression and growth signaling under nutrient-replete conditions, analogous to how elevated CDK/cyclin activity in nutrient-sensing pathways opposes longevity. Pho85 activity, when driven by its cyclins, counteracts stress-response and autophagy programs that are pro-longevity. Loss of Pho85-associated cyclins is generally associated with extended chronological or replicative lifespan in yeast, placing PCL7 in an anti-longevity role through deregulated nutrient sensing.
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 PCL7. The mechanistic reasoning is plausible and well-grounded: PCL7 encodes a Pho85-associated cyclin, and Pho85 cyclins are known to regulate nutrient-sensing pathways. The model correctly identifies that loss of Pho85-associated cyclins tends to extend lifespan, placing PCL7 in an anti-longevity role. The mechanism class of "deregulated_nutrient_sensing" is reasonable. The confidence of 0.55 is appropriately modest given the limited direct evidence for PCL7 specifically. The reasoning is coherent and mechanistically sound, though it relies somewhat on general Pho85 cyclin biology rather than PCL7-specific data.
Raw API responses
solver
{
"reasoning": "PCL7 encodes a Pho85-associated cyclin (Pcl7p) in S. cerevisiae that acts as a regulatory subunit for cyclin-dependent kinases (CDKs), specifically Pho85. Pho85 cyclins modulate nutrient-sensing pathways, including phosphate sensing and connections to the TOR/PKA nutrient-sensing network. By activating Pho85-CDK complexes, PCL7 promotes cell cycle progression and growth signaling under nutrient-replete conditions, analogous to how elevated CDK/cyclin activity in nutrient-sensing pathways opposes longevity. Pho85 activity, when driven by its cyclins, counteracts stress-response and autophagy programs that are pro-longevity. Loss of Pho85-associated cyclins is generally associated with extended chronological or replicative lifespan in yeast, placing PCL7 in an anti-longevity role through deregulated nutrient sensing.",
"confidence": 0.55,
"key_pathways": [
"Pho85-CDK nutrient sensing pathway",
"Cyclin-dependent kinase regulation",
"TOR/PKA growth signaling network"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for PCL7. The mechanistic reasoning is plausible and well-grounded: PCL7 encodes a Pho85-associated cyclin, and Pho85 cyclins are known to regulate nutrient-sensing pathways. The model correctly identifies that loss of Pho85-associated cyclins tends to extend lifespan, placing PCL7 in an anti-longevity role. The mechanism class of \"deregulated_nutrient_sensing\" is reasonable. The confidence of 0.55 is appropriately modest given the limited direct evidence for PCL7 specifically. The reasoning is coherent and mechanistically sound, though it relies somewhat on general Pho85 cyclin biology rather than PCL7-specific data.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}