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lin-14

C. elegans

Protein lin-14

What the model saw

Gene: lin-14
Organism: Caenorhabditis elegans
Known functions: Protein lin-14. RNA polymerase II transcription regulatory region sequence-specific DNA binding. double-stranded DNA binding. single-stranded DNA binding.
View unredacted entry
Protein lin-14. RNA polymerase II transcription regulatory region sequence-specific DNA binding. double-stranded DNA binding. single-stranded DNA binding.

Solver output

Predicted influence
Anti-longevity
Confidence
75%
Mechanism
Altered intercellular communication
Reasoning

LIN-14 is a transcription factor in C. elegans that functions as a master temporal regulator in the heterochronic pathway, binding RNA Pol II regulatory regions to control developmental timing. In the heterochronic pathway, lin-14 acts as an early-stage (L1/L2) transcriptional activator whose downregulation by the microRNA lin-4 is required for normal developmental progression. Persistent or elevated LIN-14 activity delays developmental transitions and is associated with retarded (younger-stage) cell fates, effectively opposing the normal aging/maturation program. Critically, loss-of-function mutations in lin-14 have been shown to extend lifespan in C. elegans, indicating that the normal function of LIN-14 is to promote aging and limit longevity. This places lin-14 in the heterochronic/temporal signaling axis, which intersects with altered intercellular communication and developmental timing control relevant to aging rate.

Key pathways
heterochronic pathway (lin-4/lin-14 axis)RNA polymerase II transcriptional regulationdevelopmental timing and temporal identity
Longevity influence
Anti-longevity
Lifespan effect
Increase

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 identified lin-14 as anti_longevity with good confidence (0.75). The mechanistic reasoning is largely correct - lin-14 is indeed a heterochronic gene and a transcription factor regulated by lin-4 miRNA, and loss-of-function mutations do extend lifespan. The mechanism class "altered_intercellular_communication" is a somewhat imprecise categorization for what is primarily a developmental timing/transcriptional regulation mechanism, but the core reasoning about the heterochronic pathway and the anti-longevity role is accurate. The model correctly notes that LIN-14 promotes aging and limits longevity, making it anti_longevity.

Raw API responses

solver

{
  "reasoning": "LIN-14 is a transcription factor in C. elegans that functions as a master temporal regulator in the heterochronic pathway, binding RNA Pol II regulatory regions to control developmental timing. In the heterochronic pathway, lin-14 acts as an early-stage (L1/L2) transcriptional activator whose downregulation by the microRNA lin-4 is required for normal developmental progression. Persistent or elevated LIN-14 activity delays developmental transitions and is associated with retarded (younger-stage) cell fates, effectively opposing the normal aging/maturation program. Critically, loss-of-function mutations in lin-14 have been shown to extend lifespan in C. elegans, indicating that the normal function of LIN-14 is to promote aging and limit longevity. This places lin-14 in the heterochronic/temporal signaling axis, which intersects with altered intercellular communication and developmental timing control relevant to aging rate.",
  "confidence": 0.75,
  "key_pathways": [
    "heterochronic pathway (lin-4/lin-14 axis)",
    "RNA polymerase II transcriptional regulation",
    "developmental timing and temporal identity"
  ],
  "mechanism_class": "altered_intercellular_communication",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly identified lin-14 as anti_longevity with good confidence (0.75). The mechanistic reasoning is largely correct - lin-14 is indeed a heterochronic gene and a transcription factor regulated by lin-4 miRNA, and loss-of-function mutations do extend lifespan. The mechanism class \"altered_intercellular_communication\" is a somewhat imprecise categorization for what is primarily a developmental timing/transcriptional regulation mechanism, but the core reasoning about the heterochronic pathway and the anti-longevity role is accurate. The model correctly notes that LIN-14 promotes aging and limits longevity, making it anti_longevity.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}