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nhr-265

C. elegans

Nuclear Hormone Receptor family

What the model saw

Gene: nhr-265
Organism: Caenorhabditis elegans
Known functions: Nuclear Hormone Receptor family. DNA-binding transcription factor activity. RNA polymerase II cis-regulatory region sequence-specific DNA binding. sequence-specific DNA binding. zinc ion binding.
View unredacted entry
Nuclear Hormone Receptor family. DNA-binding transcription factor activity. RNA polymerase II cis-regulatory region sequence-specific DNA binding. sequence-specific DNA binding. zinc ion binding.

Solver output

Predicted influence
Unclear
Confidence
35%
Mechanism
Deregulated nutrient sensing
Reasoning

nhr-265 belongs to the Nuclear Hormone Receptor (NHR) superfamily in C. elegans, which encompasses a large and functionally diverse group of ligand-regulated transcription factors. While some NHRs in C. elegans are well-characterized longevity regulators (e.g., nhr-49 modulates fatty acid metabolism and lifespan, daf-12 integrates steroid hormone signaling with dauer/longevity decisions), nhr-265 is a poorly characterized family member. Its molecular functions — sequence-specific DNA binding via zinc finger domains and RNA Pol II cis-regulatory region binding — are consistent with transcriptional regulation, but without knowledge of its specific ligand, target genes, or pathway context, the direction of its effect on longevity cannot be confidently determined. NHR family members in C. elegans can act either pro- or anti-longevity depending on whether they activate or repress metabolic, stress-response, or nutrient-sensing programs. The deregulated nutrient sensing hallmark is the best fit given the NHR superfamily's broad role in metabolic transcriptional control, but the specific role of nhr-265 remains ambiguous.

Key pathways
Nuclear hormone receptor transcriptional regulationLipid/steroid hormone signalingNutrient-sensing transcriptional networks
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
Incorrect
Mechanism
Incorrect
Reasoning quality
3/5
Failure mode
Appropriately uncertain
Notes

The model predicted "unclear" while the ground truth is "anti_longevity." The model's reasoning is sound in acknowledging that nhr-265 is poorly characterized and that NHR family members can act either pro- or anti-longevity. However, it failed to commit to a direction. The model's confidence was appropriately low (0.35), and it correctly identified the NHR superfamily context and relevant pathways. The mechanism class of "deregulated_nutrient_sensing" is a reasonable guess for an NHR but cannot be confirmed as correct. This is a case of appropriate uncertainty rather than a confident wrong answer, but the prediction is still incorrect relative to the ground truth.

Raw API responses

solver

{
  "reasoning": "nhr-265 belongs to the Nuclear Hormone Receptor (NHR) superfamily in C. elegans, which encompasses a large and functionally diverse group of ligand-regulated transcription factors. While some NHRs in C. elegans are well-characterized longevity regulators (e.g., nhr-49 modulates fatty acid metabolism and lifespan, daf-12 integrates steroid hormone signaling with dauer/longevity decisions), nhr-265 is a poorly characterized family member. Its molecular functions — sequence-specific DNA binding via zinc finger domains and RNA Pol II cis-regulatory region binding — are consistent with transcriptional regulation, but without knowledge of its specific ligand, target genes, or pathway context, the direction of its effect on longevity cannot be confidently determined. NHR family members in C. elegans can act either pro- or anti-longevity depending on whether they activate or repress metabolic, stress-response, or nutrient-sensing programs. The deregulated nutrient sensing hallmark is the best fit given the NHR superfamily's broad role in metabolic transcriptional control, but the specific role of nhr-265 remains ambiguous.",
  "confidence": 0.35,
  "key_pathways": [
    "Nuclear hormone receptor transcriptional regulation",
    "Lipid/steroid hormone signaling",
    "Nutrient-sensing transcriptional networks"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "unclear"
}

advisor

{
  "notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity.\" The model's reasoning is sound in acknowledging that nhr-265 is poorly characterized and that NHR family members can act either pro- or anti-longevity. However, it failed to commit to a direction. The model's confidence was appropriately low (0.35), and it correctly identified the NHR superfamily context and relevant pathways. The mechanism class of \"deregulated_nutrient_sensing\" is a reasonable guess for an NHR but cannot be confirmed as correct. This is a case of appropriate uncertainty rather than a confident wrong answer, but the prediction is still incorrect relative to the ground truth.",
  "failure_mode": "appropriately_uncertain",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}