ndab-1
C. elegans
Acyl carrier protein
What the model saw
Gene: ndab-1 Organism: Caenorhabditis elegans Known functions: Acyl carrier protein. acyl binding. acyl carrier activity.
View unredacted entry
Acyl carrier protein. acyl binding. acyl carrier activity.
Solver output
ndab-1 encodes an acyl carrier protein (ACP) in C. elegans, which plays a central role in fatty acid biosynthesis by covalently shuttling acyl intermediates via its phosphopantetheine prosthetic group through the fatty acid synthase (FAS) complex. Proper acyl carrier activity is essential for de novo lipid synthesis and lipid homeostasis, which are tightly coupled to nutrient-sensing pathways (e.g., TORC1, insulin/IGF-1 signaling) that regulate longevity. In C. elegans, perturbations in fatty acid composition and lipid metabolism—particularly involving mitochondrial and cytosolic ACPs—have been linked to altered lifespan, often through effects on mitochondrial function and membrane lipid remodeling. Mitochondrial ACP (mt-ACP) is also known to be a component of the mitochondrial respiratory chain assembly and lipoic acid synthesis, connecting it to mitochondrial integrity. Loss of ACP function typically disrupts lipid homeostasis and mitochondrial function, which would be detrimental to longevity, implying the normal function is pro-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 reasoned that loss of ACP function would be detrimental (implying normal function is pro-longevity), but the ground truth indicates ndab-1 is anti-longevity, meaning its normal function reduces lifespan (or its loss extends lifespan). The model's mechanistic reasoning about fatty acid biosynthesis and mitochondrial ACP is plausible in general terms but led to the wrong conclusion. The model had low confidence (0.52) but still got the direction wrong. The reasoning quality is poor because it failed to consider that acyl carrier proteins involved in lipid synthesis could promote aging (e.g., through lipid accumulation or lipotoxicity), which is the actual biological outcome.
Raw API responses
solver
{
"reasoning": "ndab-1 encodes an acyl carrier protein (ACP) in C. elegans, which plays a central role in fatty acid biosynthesis by covalently shuttling acyl intermediates via its phosphopantetheine prosthetic group through the fatty acid synthase (FAS) complex. Proper acyl carrier activity is essential for de novo lipid synthesis and lipid homeostasis, which are tightly coupled to nutrient-sensing pathways (e.g., TORC1, insulin/IGF-1 signaling) that regulate longevity. In C. elegans, perturbations in fatty acid composition and lipid metabolism—particularly involving mitochondrial and cytosolic ACPs—have been linked to altered lifespan, often through effects on mitochondrial function and membrane lipid remodeling. Mitochondrial ACP (mt-ACP) is also known to be a component of the mitochondrial respiratory chain assembly and lipoic acid synthesis, connecting it to mitochondrial integrity. Loss of ACP function typically disrupts lipid homeostasis and mitochondrial function, which would be detrimental to longevity, implying the normal function is pro-longevity.",
"confidence": 0.52,
"key_pathways": [
"fatty acid biosynthesis / lipid homeostasis",
"mitochondrial ACP / lipoic acid synthesis",
"nutrient sensing (TORC1/insulin-IGF-1 signaling)"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model reasoned that loss of ACP function would be detrimental (implying normal function is pro-longevity), but the ground truth indicates ndab-1 is anti-longevity, meaning its normal function reduces lifespan (or its loss extends lifespan). The model's mechanistic reasoning about fatty acid biosynthesis and mitochondrial ACP is plausible in general terms but led to the wrong conclusion. The model had low confidence (0.52) but still got the direction wrong. The reasoning quality is poor because it failed to consider that acyl carrier proteins involved in lipid synthesis could promote aging (e.g., through lipid accumulation or lipotoxicity), which is the actual biological outcome.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}