YTA7
S. cerevisiae
chromatin segregase YTA7
What the model saw
Gene: YTA7 Organism: Saccharomyces cerevisiae Known functions: chromatin segregase YTA7. ATP binding. ATP hydrolysis activity. ATP-dependent chromatin remodeler activity. ATP-dependent histone chaperone activity. chromatin binding. histone binding.
View unredacted entry
chromatin segregase YTA7. ATP binding. ATP hydrolysis activity. ATP-dependent chromatin remodeler activity. ATP-dependent histone chaperone activity. chromatin binding. histone binding.
Solver output
YTA7 is an ATP-dependent chromatin remodeler and histone chaperone that functions as a chromatin segregase, using ATP hydrolysis to disassemble or reorganize nucleosomes. Proper chromatin remodeling and histone chaperoning are essential for maintaining epigenetic fidelity during DNA replication and transcription. Loss of chromatin integrity and aberrant histone deposition are hallmarks of epigenetic dysregulation associated with aging in yeast. YTA7 specifically helps prevent inappropriate histone deposition and maintains chromatin boundaries, which supports transcriptional fidelity and suppresses genomic noise that accumulates with age. By preserving ordered chromatin states through its ATP-dependent histone chaperone activity, YTA7's normal function would be expected to oppose age-related epigenetic drift and promote longevity.
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 model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — it correctly identifies YTA7's role as an ATP-dependent chromatin remodeler and histone chaperone — but it incorrectly infers that these functions would promote longevity. In reality, YTA7 is anti-longevity in yeast, meaning its deletion or loss likely extends lifespan. The model failed to consider that chromatin remodelers can sometimes act as anti-longevity factors, for example by promoting transcription of genes that accelerate aging or by disrupting silencing at rDNA loci. The model's confidence of 0.62 is moderate but still committed to the wrong answer. The mechanistic reasoning, while internally consistent, leads to the wrong conclusion and does not reflect the actual biology of YTA7 in yeast aging.
Raw API responses
solver
{
"reasoning": "YTA7 is an ATP-dependent chromatin remodeler and histone chaperone that functions as a chromatin segregase, using ATP hydrolysis to disassemble or reorganize nucleosomes. Proper chromatin remodeling and histone chaperoning are essential for maintaining epigenetic fidelity during DNA replication and transcription. Loss of chromatin integrity and aberrant histone deposition are hallmarks of epigenetic dysregulation associated with aging in yeast. YTA7 specifically helps prevent inappropriate histone deposition and maintains chromatin boundaries, which supports transcriptional fidelity and suppresses genomic noise that accumulates with age. By preserving ordered chromatin states through its ATP-dependent histone chaperone activity, YTA7's normal function would be expected to oppose age-related epigenetic drift and promote longevity.",
"confidence": 0.62,
"key_pathways": [
"ATP-dependent chromatin remodeling",
"histone chaperone activity / nucleosome assembly",
"epigenetic maintenance / chromatin boundary establishment"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — it correctly identifies YTA7's role as an ATP-dependent chromatin remodeler and histone chaperone — but it incorrectly infers that these functions would promote longevity. In reality, YTA7 is anti-longevity in yeast, meaning its deletion or loss likely extends lifespan. The model failed to consider that chromatin remodelers can sometimes act as anti-longevity factors, for example by promoting transcription of genes that accelerate aging or by disrupting silencing at rDNA loci. The model's confidence of 0.62 is moderate but still committed to the wrong answer. The mechanistic reasoning, while internally consistent, leads to the wrong conclusion and does not reflect the actual biology of YTA7 in yeast aging.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}