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CLN3

S. cerevisiae

cyclin CLN3

What the model saw

Gene: CLN3
Organism: Saccharomyces cerevisiae
Known functions: cyclin CLN3. cyclin-dependent protein serine/threonine kinase regulator activity. protein binding.
View unredacted entry
cyclin CLN3. cyclin-dependent protein serine/threonine kinase regulator activity. protein binding.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

CLN3 encodes a G1 cyclin in S. cerevisiae that acts as a regulatory subunit for the cyclin-dependent kinase Cdc28 (CDK1), promoting passage through Start and commitment to cell division. CLN3 is a key integrator of nutrient and growth signals: it is stabilized by high TOR/PKA activity and drives cells into the cell cycle under favorable conditions. Elevated CLN3 activity accelerates cell cycle entry and promotes growth, which is associated with shortened chronological and replicative lifespan in yeast — analogous to how hyperactive nutrient-sensing (TOR, RAS/PKA) shortens lifespan. Conversely, reduced CLN3 activity or delayed Start is associated with extended lifespan, consistent with the pro-longevity effects of nutrient restriction and reduced CDK activity. CLN3 thus functions as a pro-growth, pro-proliferative signal that opposes longevity by coupling nutrient availability to cell cycle progression.

Key pathways
TOR/PKA nutrient sensing → CLN3 stabilization → CDK1 activation → G1/S transitionCdc28-CLN3 cyclin-dependent kinase complex at StartReplicative and chronological lifespan regulation via cell cycle entry
Longevity influence
Anti-longevity
Lifespan effect
Decrease

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

Answer
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted CLN3 as anti_longevity with good confidence (0.72). The mechanistic reasoning is sound: CLN3 is a G1 cyclin that promotes cell cycle entry via CDK1/Cdc28, and its pro-growth activity is associated with shortened lifespan. The connection to nutrient sensing (TOR/PKA) is reasonable and well-established in yeast biology. The reasoning is coherent and biologically accurate, though the specific experimental evidence for CLN3's effect on yeast lifespan could have been cited more directly rather than relying on analogical reasoning from nutrient sensing pathways.

Raw API responses

solver

{
  "reasoning": "CLN3 encodes a G1 cyclin in S. cerevisiae that acts as a regulatory subunit for the cyclin-dependent kinase Cdc28 (CDK1), promoting passage through Start and commitment to cell division. CLN3 is a key integrator of nutrient and growth signals: it is stabilized by high TOR/PKA activity and drives cells into the cell cycle under favorable conditions. Elevated CLN3 activity accelerates cell cycle entry and promotes growth, which is associated with shortened chronological and replicative lifespan in yeast — analogous to how hyperactive nutrient-sensing (TOR, RAS/PKA) shortens lifespan. Conversely, reduced CLN3 activity or delayed Start is associated with extended lifespan, consistent with the pro-longevity effects of nutrient restriction and reduced CDK activity. CLN3 thus functions as a pro-growth, pro-proliferative signal that opposes longevity by coupling nutrient availability to cell cycle progression.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR/PKA nutrient sensing → CLN3 stabilization → CDK1 activation → G1/S transition",
    "Cdc28-CLN3 cyclin-dependent kinase complex at Start",
    "Replicative and chronological lifespan regulation via cell cycle entry"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted CLN3 as anti_longevity with good confidence (0.72). The mechanistic reasoning is sound: CLN3 is a G1 cyclin that promotes cell cycle entry via CDK1/Cdc28, and its pro-growth activity is associated with shortened lifespan. The connection to nutrient sensing (TOR/PKA) is reasonable and well-established in yeast biology. The reasoning is coherent and biologically accurate, though the specific experimental evidence for CLN3's effect on yeast lifespan could have been cited more directly rather than relying on analogical reasoning from nutrient sensing pathways.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}