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lin-15B

C. elegans

Protein lin-15B

What the model saw

Gene: lin-15B
Organism: Caenorhabditis elegans
Known functions: Protein lin-15B. signaling receptor binding.
View unredacted entry
Protein lin-15B. signaling receptor binding.

Solver output

Predicted influence
Pro-longevity
Confidence
52%
Mechanism
Epigenetic alterations
Reasoning

lin-15B in C. elegans is a synthetic multivulva (synMuv) class B gene that encodes a transcriptional repressor functioning as part of the DRM/DREAM complex, which represses germline and somatic gene expression programs. Loss of lin-15B has been shown to extend lifespan in C. elegans by derepressing stress-response and longevity-associated transcriptional programs, suggesting its normal function is to repress pro-longevity gene expression. Its annotation as a signaling receptor binding protein is consistent with its role in modulating transcriptional repressor complexes that interface with signaling pathways. The DREAM complex in C. elegans coordinates chromatin-level silencing, placing lin-15B squarely in the epigenetic alterations hallmark. Because lin-15B's normal activity suppresses longevity-promoting transcription, its wild-type function is anti-longevity, meaning loss-of-function extends lifespan — so the gene itself is anti-longevity.

Key pathways
DRM/DREAM transcriptional repressor complexsynMuv B chromatin silencingsignaling receptor-coupled transcriptional regulation
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

The advisor flagged this ground-truth label as potentially questionable.
Answer
Correct
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Right answer, wrong reasoning
Notes

The model correctly predicts "pro_longevity" as the longevity influence, matching the ground truth. However, the reasoning is internally contradictory and ultimately wrong in its mechanistic conclusion. The model correctly identifies lin-15B as a synMuv B transcriptional repressor in the DRM/DREAM complex, and correctly notes that loss-of-function extends lifespan. But then it contradicts itself: it first says lin-15B's normal function is "anti-longevity" (because loss-of-function extends lifespan), but then outputs "pro_longevity" as the final answer. The GenAge classification of "pro_longevity" for lin-15B is actually consistent with the interpretation that the gene promotes longevity — but the model's own reasoning argues the opposite (that it's anti-longevity). The model arrives at the correct answer despite its reasoning pointing to the opposite conclusion, suggesting the final answer may have been influenced by prior knowledge or a guess rather than the stated reasoning. The mechanism class of "epigenetic_alterations" is plausible but the reasoning is self-contradictory and confused about the directionality of the longevity effect.

Raw API responses

solver

{
  "reasoning": "lin-15B in C. elegans is a synthetic multivulva (synMuv) class B gene that encodes a transcriptional repressor functioning as part of the DRM/DREAM complex, which represses germline and somatic gene expression programs. Loss of lin-15B has been shown to extend lifespan in C. elegans by derepressing stress-response and longevity-associated transcriptional programs, suggesting its normal function is to repress pro-longevity gene expression. Its annotation as a signaling receptor binding protein is consistent with its role in modulating transcriptional repressor complexes that interface with signaling pathways. The DREAM complex in C. elegans coordinates chromatin-level silencing, placing lin-15B squarely in the epigenetic alterations hallmark. Because lin-15B's normal activity suppresses longevity-promoting transcription, its wild-type function is anti-longevity, meaning loss-of-function extends lifespan — so the gene itself is anti-longevity.",
  "confidence": 0.52,
  "key_pathways": [
    "DRM/DREAM transcriptional repressor complex",
    "synMuv B chromatin silencing",
    "signaling receptor-coupled transcriptional regulation"
  ],
  "mechanism_class": "epigenetic_alterations",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicts \"pro_longevity\" as the longevity influence, matching the ground truth. However, the reasoning is internally contradictory and ultimately wrong in its mechanistic conclusion. The model correctly identifies lin-15B as a synMuv B transcriptional repressor in the DRM/DREAM complex, and correctly notes that loss-of-function extends lifespan. But then it contradicts itself: it first says lin-15B's normal function is \"anti-longevity\" (because loss-of-function extends lifespan), but then outputs \"pro_longevity\" as the final answer. The GenAge classification of \"pro_longevity\" for lin-15B is actually consistent with the interpretation that the gene promotes longevity — but the model's own reasoning argues the opposite (that it's anti-longevity). The model arrives at the correct answer despite its reasoning pointing to the opposite conclusion, suggesting the final answer may have been influenced by prior knowledge or a guess rather than the stated reasoning. The mechanism class of \"epigenetic_alterations\" is plausible but the reasoning is self-contradictory and confused about the directionality of the longevity effect.",
  "failure_mode": "right_answer_wrong_reasoning",
  "answer_correct": true,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": true
}