cchl-1
C. elegans
putative holocytochrome-c-type synthase
What the model saw
Gene: cchl-1 Organism: Caenorhabditis elegans Known functions: putative holocytochrome-c-type synthase. holocytochrome-c synthase activity.
View unredacted entry
putative holocytochrome-c-type synthase. holocytochrome-c synthase activity.
Solver output
Holocytochrome-c synthase (HCCS) catalyzes the covalent attachment of heme to apocytochrome c, producing mature holocytochrome c, which is an essential electron carrier in the mitochondrial respiratory chain (Complex III to Complex IV). Proper cytochrome c maturation is required for efficient oxidative phosphorylation and mitochondrial electron transport chain function. Loss of cchl-1 function would impair mitochondrial respiration, reduce ATP production, and potentially increase reactive oxygen species leakage — all hallmarks of mitochondrial dysfunction associated with accelerated aging. Conversely, normal cchl-1 activity supports mitochondrial integrity and efficient energy metabolism, which is generally pro-longevity in C. elegans. While some mitochondrial perturbations in C. elegans paradoxically extend lifespan via mitohormesis, the core role of HCCS in maintaining electron transport chain competency aligns more strongly with supporting healthy mitochondrial function and 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 correctly identifies the biochemical function of cchl-1 (holocytochrome-c synthase, heme attachment to cytochrome c, ETC function), but draws the wrong conclusion about its longevity influence. The model acknowledged the mitohormesis paradox in C. elegans (where mitochondrial perturbations can extend lifespan) but dismissed it in favor of the "normal function supports longevity" argument. In reality, cchl-1 is anti_longevity, meaning its loss or reduction likely extends lifespan — consistent with the well-documented mitohormesis phenomenon in C. elegans where partial impairment of the mitochondrial ETC extends lifespan. The model was moderately confident (0.72) in the wrong direction. The mechanistic reasoning about the gene's biochemical role is accurate, but the inference about longevity direction is incorrect.
Raw API responses
solver
{
"reasoning": "Holocytochrome-c synthase (HCCS) catalyzes the covalent attachment of heme to apocytochrome c, producing mature holocytochrome c, which is an essential electron carrier in the mitochondrial respiratory chain (Complex III to Complex IV). Proper cytochrome c maturation is required for efficient oxidative phosphorylation and mitochondrial electron transport chain function. Loss of cchl-1 function would impair mitochondrial respiration, reduce ATP production, and potentially increase reactive oxygen species leakage — all hallmarks of mitochondrial dysfunction associated with accelerated aging. Conversely, normal cchl-1 activity supports mitochondrial integrity and efficient energy metabolism, which is generally pro-longevity in C. elegans. While some mitochondrial perturbations in C. elegans paradoxically extend lifespan via mitohormesis, the core role of HCCS in maintaining electron transport chain competency aligns more strongly with supporting healthy mitochondrial function and longevity.",
"confidence": 0.72,
"key_pathways": [
"mitochondrial electron transport chain (Complex III–IV)",
"cytochrome c maturation/heme attachment",
"oxidative phosphorylation"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning correctly identifies the biochemical function of cchl-1 (holocytochrome-c synthase, heme attachment to cytochrome c, ETC function), but draws the wrong conclusion about its longevity influence. The model acknowledged the mitohormesis paradox in C. elegans (where mitochondrial perturbations can extend lifespan) but dismissed it in favor of the \"normal function supports longevity\" argument. In reality, cchl-1 is anti_longevity, meaning its loss or reduction likely extends lifespan — consistent with the well-documented mitohormesis phenomenon in C. elegans where partial impairment of the mitochondrial ETC extends lifespan. The model was moderately confident (0.72) in the wrong direction. The mechanistic reasoning about the gene's biochemical role is accurate, but the inference about longevity direction is incorrect.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}