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bra-1

C. elegans

MYND-type domain-containing protein

What the model saw

Gene: bra-1
Organism: Caenorhabditis elegans
Known functions: MYND-type domain-containing protein. histone H3 reader activity. protein binding. signaling receptor binding. transcription corepressor activity. zinc ion binding.
View unredacted entry
MYND-type domain-containing protein. histone H3 reader activity. protein binding. signaling receptor binding. transcription corepressor activity. zinc ion binding.

Solver output

Predicted influence
Anti-longevity
Confidence
62%
Mechanism
Epigenetic alterations
Reasoning

bra-1 encodes a MYND-type zinc finger domain-containing protein with histone H3 reader activity and transcription corepressor activity. MYND domains are known to recruit co-repressor complexes (e.g., NuRD/HDAC complexes) to chromatin, silencing gene expression. As a histone H3 reader, bra-1 likely recognizes specific histone marks to direct transcriptional repression of target genes. If bra-1 acts as a corepressor of pro-longevity transcription factors (such as DAF-16/FOXO or stress-response genes), its normal function would suppress longevity-promoting transcriptional programs. MYND-domain corepressors in other organisms have been shown to antagonize nuclear hormone receptor and FOXO signaling, which are central to lifespan extension in C. elegans. Thus, the normal function of bra-1 is predicted to oppose longevity by epigenetically silencing pro-longevity gene expression.

Key pathways
histone H3 reading and chromatin-mediated transcriptional repressionDAF-16/FOXO transcriptional corepressionMYND-domain corepressor complex recruitment
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 was plausible on the surface (MYND-domain corepressors silencing pro-longevity genes like DAF-16/FOXO), but it reached the wrong conclusion. The model assumed that a transcription corepressor would necessarily suppress longevity pathways, but bra-1 appears to actually promote longevity in C. elegans. The mechanistic reasoning was speculative and incorrect - bra-1 likely acts as a corepressor of anti-longevity genes or promotes longevity through other mechanisms. The model had moderate confidence (0.62) in the wrong direction.

Raw API responses

solver

{
  "reasoning": "bra-1 encodes a MYND-type zinc finger domain-containing protein with histone H3 reader activity and transcription corepressor activity. MYND domains are known to recruit co-repressor complexes (e.g., NuRD/HDAC complexes) to chromatin, silencing gene expression. As a histone H3 reader, bra-1 likely recognizes specific histone marks to direct transcriptional repression of target genes. If bra-1 acts as a corepressor of pro-longevity transcription factors (such as DAF-16/FOXO or stress-response genes), its normal function would suppress longevity-promoting transcriptional programs. MYND-domain corepressors in other organisms have been shown to antagonize nuclear hormone receptor and FOXO signaling, which are central to lifespan extension in C. elegans. Thus, the normal function of bra-1 is predicted to oppose longevity by epigenetically silencing pro-longevity gene expression.",
  "confidence": 0.62,
  "key_pathways": [
    "histone H3 reading and chromatin-mediated transcriptional repression",
    "DAF-16/FOXO transcriptional corepression",
    "MYND-domain corepressor complex recruitment"
  ],
  "mechanism_class": "epigenetic_alterations",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model predicted anti_longevity but the ground truth is pro_longevity. The model's reasoning was plausible on the surface (MYND-domain corepressors silencing pro-longevity genes like DAF-16/FOXO), but it reached the wrong conclusion. The model assumed that a transcription corepressor would necessarily suppress longevity pathways, but bra-1 appears to actually promote longevity in C. elegans. The mechanistic reasoning was speculative and incorrect - bra-1 likely acts as a corepressor of anti-longevity genes or promotes longevity through other mechanisms. The model had moderate confidence (0.62) in the wrong direction.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}