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cdk-7

C. elegans

Cyclin-dependent kinase 7

What the model saw

Gene: cdk-7
Organism: Caenorhabditis elegans
Known functions: Cyclin-dependent kinase 7. ATP binding. RNA polymerase II CTD heptapeptide repeat kinase activity. cyclin-dependent protein serine/threonine kinase activity. protein kinase activity. protein serine kinase activity.
View unredacted entry
Cyclin-dependent kinase 7. ATP binding. RNA polymerase II CTD heptapeptide repeat kinase activity. cyclin-dependent protein serine/threonine kinase activity. protein kinase activity. protein serine kinase activity.

Solver output

Predicted influence
Anti-longevity
Confidence
65%
Mechanism
Deregulated nutrient sensing
Reasoning

CDK-7 is the C. elegans ortholog of CDK7, the catalytic subunit of the CDK-activating kinase (CAK) complex. It phosphorylates the T-loop of cell-cycle CDKs (CDK1, CDK2, CDK4/6), activating them to drive cell proliferation. Additionally, CDK-7 phosphorylates the heptapeptide repeat of the RNA Pol II CTD (Ser5/Ser7), licensing transcription initiation and coupling it to mRNA capping. Elevated CDK activity and enhanced proliferative/transcriptional output are generally associated with reduced longevity in C. elegans, as reduced CDK activity (e.g., via reduced germline proliferation signaling) is a well-established pro-longevity intervention. CDK-7's role in activating CDK-1 and CDK-2 also connects it to the germline proliferation axis, where dampening this pathway extends lifespan. Furthermore, CDK7-mediated RNA Pol II CTD phosphorylation drives global transcriptional output, and reduced transcription is associated with longevity in multiple model organisms.

Key pathways
CDK-activating kinase (CAK) / cell cycle CDK activationRNA Polymerase II CTD phosphorylation / transcription initiationGermline proliferation signaling
Longevity influence
Pro-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
Incorrect
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Confident wrong
Notes

The model predicted anti_longevity but the ground truth is pro_longevity. The model's reasoning is based on a general assumption that elevated CDK activity reduces longevity, but this is incorrect for cdk-7 in C. elegans. CDK-7 in C. elegans has been shown to promote longevity, likely through its role in transcriptional regulation (RNA Pol II CTD phosphorylation) rather than simply driving proliferation. The model's mechanistic reasoning is also misclassified as "deregulated_nutrient_sensing" when CDK-7 is primarily involved in cell cycle regulation and transcription. The model's logic that "elevated CDK activity = reduced longevity" is an oversimplification that leads to the wrong conclusion. The model was moderately confident (0.65) in the wrong direction.

Raw API responses

solver

{
  "reasoning": "CDK-7 is the C. elegans ortholog of CDK7, the catalytic subunit of the CDK-activating kinase (CAK) complex. It phosphorylates the T-loop of cell-cycle CDKs (CDK1, CDK2, CDK4/6), activating them to drive cell proliferation. Additionally, CDK-7 phosphorylates the heptapeptide repeat of the RNA Pol II CTD (Ser5/Ser7), licensing transcription initiation and coupling it to mRNA capping. Elevated CDK activity and enhanced proliferative/transcriptional output are generally associated with reduced longevity in C. elegans, as reduced CDK activity (e.g., via reduced germline proliferation signaling) is a well-established pro-longevity intervention. CDK-7's role in activating CDK-1 and CDK-2 also connects it to the germline proliferation axis, where dampening this pathway extends lifespan. Furthermore, CDK7-mediated RNA Pol II CTD phosphorylation drives global transcriptional output, and reduced transcription is associated with longevity in multiple model organisms.",
  "confidence": 0.65,
  "key_pathways": [
    "CDK-activating kinase (CAK) / cell cycle CDK activation",
    "RNA Polymerase II CTD phosphorylation / transcription initiation",
    "Germline proliferation signaling"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model predicted anti_longevity but the ground truth is pro_longevity. The model's reasoning is based on a general assumption that elevated CDK activity reduces longevity, but this is incorrect for cdk-7 in C. elegans. CDK-7 in C. elegans has been shown to promote longevity, likely through its role in transcriptional regulation (RNA Pol II CTD phosphorylation) rather than simply driving proliferation. The model's mechanistic reasoning is also misclassified as \"deregulated_nutrient_sensing\" when CDK-7 is primarily involved in cell cycle regulation and transcription. The model's logic that \"elevated CDK activity = reduced longevity\" is an oversimplification that leads to the wrong conclusion. The model was moderately confident (0.65) in the wrong direction.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}