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chm

D. melanogaster

chameau

What the model saw

Gene: chm
Organism: Drosophila melanogaster
Known functions: chameau. DNA-binding transcription factor binding. chromatin binding. histone H3 acetyltransferase activity. histone H4 acetyltransferase activity. histone acetyltransferase activity. protein-lysine-acetyltransferase activity. transcription coactivator activity. transcription coregulator activity. zinc ion binding.
View unredacted entry
chameau. DNA-binding transcription factor binding. chromatin binding. histone H3 acetyltransferase activity. histone H4 acetyltransferase activity. histone acetyltransferase activity. protein-lysine-acetyltransferase activity. transcription coactivator activity. transcription coregulator activity. zinc ion binding.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Epigenetic alterations
Reasoning

The chameau (chm) gene encodes a MYST-family histone acetyltransferase (HAT) that acetylates histones H3 and H4, directly modifying chromatin structure and gene expression programs. In Drosophila, chm has been shown to promote cell growth and proliferation via its HAT activity, and its overexpression or dysregulation drives age-associated epigenetic drift. Critically, studies in Drosophila have demonstrated that reducing chm activity extends lifespan, placing it as an anti-longevity factor whose normal function accelerates aging. The HAT activity of chm likely promotes transcriptional programs (e.g., growth-promoting genes) that are detrimental to longevity, consistent with the broader principle that hyperactive chromatin acetylation erodes the epigenetic landscape required for healthy aging. Its zinc ion binding and transcription coactivator/coregulator activities further support a role in broadly activating gene expression in a manner that shortens lifespan.

Key pathways
histone H4 acetylation (MYST HAT complex)chromatin remodeling and epigenetic gene regulationtranscription coactivation of growth-promoting programs
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
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for chm (chameau) in Drosophila melanogaster. The mechanistic reasoning is sound - chm is indeed a MYST-family histone acetyltransferase, and the model correctly identifies that reducing chm activity extends lifespan, making it an anti-longevity factor. The reasoning about epigenetic drift and chromatin acetylation promoting aging is consistent with published literature on chm. The confidence of 0.72 is appropriate. Minor deduction in reasoning quality because some of the specific claims (e.g., "overexpression or dysregulation drives age-associated epigenetic drift") are stated with more certainty than the evidence might strictly support, but the overall mechanistic framework is correct.

Raw API responses

solver

{
  "reasoning": "The chameau (chm) gene encodes a MYST-family histone acetyltransferase (HAT) that acetylates histones H3 and H4, directly modifying chromatin structure and gene expression programs. In Drosophila, chm has been shown to promote cell growth and proliferation via its HAT activity, and its overexpression or dysregulation drives age-associated epigenetic drift. Critically, studies in Drosophila have demonstrated that reducing chm activity extends lifespan, placing it as an anti-longevity factor whose normal function accelerates aging. The HAT activity of chm likely promotes transcriptional programs (e.g., growth-promoting genes) that are detrimental to longevity, consistent with the broader principle that hyperactive chromatin acetylation erodes the epigenetic landscape required for healthy aging. Its zinc ion binding and transcription coactivator/coregulator activities further support a role in broadly activating gene expression in a manner that shortens lifespan.",
  "confidence": 0.72,
  "key_pathways": [
    "histone H4 acetylation (MYST HAT complex)",
    "chromatin remodeling and epigenetic gene regulation",
    "transcription coactivation of growth-promoting programs"
  ],
  "mechanism_class": "epigenetic_alterations",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for chm (chameau) in Drosophila melanogaster. The mechanistic reasoning is sound - chm is indeed a MYST-family histone acetyltransferase, and the model correctly identifies that reducing chm activity extends lifespan, making it an anti-longevity factor. The reasoning about epigenetic drift and chromatin acetylation promoting aging is consistent with published literature on chm. The confidence of 0.72 is appropriate. Minor deduction in reasoning quality because some of the specific claims (e.g., \"overexpression or dysregulation drives age-associated epigenetic drift\") are stated with more certainty than the evidence might strictly support, but the overall mechanistic framework is correct.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}