BMH1
S. cerevisiae
14-3-3 family protein BMH1
What the model saw
Gene: BMH1 Organism: Saccharomyces cerevisiae Known functions: 14-3-3 family protein BMH1. DNA replication origin binding. RNA polymerase II-specific DNA-binding transcription factor binding. enzyme activator activity. phosphoserine residue binding. protein binding.
View unredacted entry
14-3-3 family protein BMH1. DNA replication origin binding. RNA polymerase II-specific DNA-binding transcription factor binding. enzyme activator activity. phosphoserine residue binding. protein binding.
Solver output
BMH1 is a yeast 14-3-3 family protein that binds phosphoserine residues and acts as an enzyme activator, placing it as a central scaffold in nutrient-sensing and stress-response signaling. 14-3-3 proteins in yeast are well-established regulators of the TORC1 and Ras/PKA pathways, where they modulate the activity of key effectors such as Sch9 and Msn2/Msn4 by binding phosphorylated targets. BMH1's role in DNA replication origin binding and transcription factor binding further supports genome maintenance and transcriptional regulation under stress. Loss of BMH1 in yeast impairs proper regulation of these nutrient-sensing cascades and reduces chronological and replicative lifespan, while its normal function helps restrain pro-aging signals and support stress-response transcription. Its phosphoserine-binding and enzyme activator activities are consistent with a pro-longevity scaffolding role that coordinates multiple hallmark pathways.
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 ground truth classifies BMH1's longevity influence as "unclear," but the model confidently predicted "pro_longevity" with 0.72 confidence. The model constructed a plausible-sounding mechanistic narrative about 14-3-3 proteins in TORC1/Ras-PKA signaling, but this reasoning is speculative and not supported by the actual GenAge classification. The claim that "loss of BMH1 reduces chronological and replicative lifespan" appears to be a hallucinated specific — the GenAge entry marks the influence as unclear, suggesting the evidence is ambiguous or contradictory. The model over-committed to a definitive pro-longevity classification when the evidence does not support such a conclusion.
Raw API responses
solver
{
"reasoning": "BMH1 is a yeast 14-3-3 family protein that binds phosphoserine residues and acts as an enzyme activator, placing it as a central scaffold in nutrient-sensing and stress-response signaling. 14-3-3 proteins in yeast are well-established regulators of the TORC1 and Ras/PKA pathways, where they modulate the activity of key effectors such as Sch9 and Msn2/Msn4 by binding phosphorylated targets. BMH1's role in DNA replication origin binding and transcription factor binding further supports genome maintenance and transcriptional regulation under stress. Loss of BMH1 in yeast impairs proper regulation of these nutrient-sensing cascades and reduces chronological and replicative lifespan, while its normal function helps restrain pro-aging signals and support stress-response transcription. Its phosphoserine-binding and enzyme activator activities are consistent with a pro-longevity scaffolding role that coordinates multiple hallmark pathways.",
"confidence": 0.72,
"key_pathways": [
"TORC1/Ras-PKA nutrient sensing",
"phosphoserine-dependent signal scaffolding (14-3-3)",
"DNA replication origin regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The ground truth classifies BMH1's longevity influence as \"unclear,\" but the model confidently predicted \"pro_longevity\" with 0.72 confidence. The model constructed a plausible-sounding mechanistic narrative about 14-3-3 proteins in TORC1/Ras-PKA signaling, but this reasoning is speculative and not supported by the actual GenAge classification. The claim that \"loss of BMH1 reduces chronological and replicative lifespan\" appears to be a hallucinated specific — the GenAge entry marks the influence as unclear, suggesting the evidence is ambiguous or contradictory. The model over-committed to a definitive pro-longevity classification when the evidence does not support such a conclusion.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}