ant-1.1
C. elegans
ADP/ATP translocase
What the model saw
Gene: ant-1.1 Organism: Caenorhabditis elegans Known functions: ADP/ATP translocase. ATP:ADP antiporter activity. protein binding.
View unredacted entry
ADP/ATP translocase. ATP:ADP antiporter activity. protein binding.
Solver output
ANT-1.1 is the C. elegans adenine nucleotide translocase (ANT), which exchanges mitochondrial ATP for cytosolic ADP across the inner mitochondrial membrane, directly coupling oxidative phosphorylation to cellular energy supply. Efficient ATP/ADP exchange is essential for maintaining mitochondrial membrane potential and preventing electron leak that generates reactive oxygen species. In C. elegans, mild mitochondrial dysfunction (as seen in isp-1 or clk-1 mutants) can paradoxically extend lifespan via mitohormesis, but complete loss of ANT function typically collapses the mitochondrial membrane potential, impairs ATP synthesis, and promotes apoptosis/necrosis. The normal (wild-type) function of ant-1.1 in sustaining efficient mitochondrial energy transduction is therefore expected to support organismal health and longevity by preventing energy crisis and oxidative damage. Loss-of-function of ANT homologs in other organisms is associated with mitochondrial myopathy and accelerated aging phenotypes, further supporting a pro-longevity role for the normal gene product.
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 partially sound in describing ANT-1.1's biochemical function (ADP/ATP exchange across the inner mitochondrial membrane), but it reaches the wrong conclusion. In C. elegans, ant-1.1 is actually anti-longevity, meaning its normal activity shortens lifespan or its reduction extends lifespan. This fits with the mitohormesis framework the model itself mentions — mild mitochondrial dysfunction (including reduced ANT activity) can extend lifespan in C. elegans. The model acknowledged this possibility but then dismissed it in favor of the pro-longevity interpretation, citing loss-of-function phenotypes in other organisms. The model's confidence of 0.62 is moderate but still wrong. The mechanistic reasoning is partially correct in describing the biochemistry but fails to correctly apply the C. elegans-specific context where reduced mitochondrial efficiency often extends lifespan.
Raw API responses
solver
{
"reasoning": "ANT-1.1 is the C. elegans adenine nucleotide translocase (ANT), which exchanges mitochondrial ATP for cytosolic ADP across the inner mitochondrial membrane, directly coupling oxidative phosphorylation to cellular energy supply. Efficient ATP/ADP exchange is essential for maintaining mitochondrial membrane potential and preventing electron leak that generates reactive oxygen species. In C. elegans, mild mitochondrial dysfunction (as seen in isp-1 or clk-1 mutants) can paradoxically extend lifespan via mitohormesis, but complete loss of ANT function typically collapses the mitochondrial membrane potential, impairs ATP synthesis, and promotes apoptosis/necrosis. The normal (wild-type) function of ant-1.1 in sustaining efficient mitochondrial energy transduction is therefore expected to support organismal health and longevity by preventing energy crisis and oxidative damage. Loss-of-function of ANT homologs in other organisms is associated with mitochondrial myopathy and accelerated aging phenotypes, further supporting a pro-longevity role for the normal gene product.",
"confidence": 0.62,
"key_pathways": [
"mitochondrial ATP/ADP exchange",
"oxidative phosphorylation coupling",
"mitochondrial membrane potential maintenance"
],
"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 is partially sound in describing ANT-1.1's biochemical function (ADP/ATP exchange across the inner mitochondrial membrane), but it reaches the wrong conclusion. In C. elegans, ant-1.1 is actually anti-longevity, meaning its normal activity shortens lifespan or its reduction extends lifespan. This fits with the mitohormesis framework the model itself mentions — mild mitochondrial dysfunction (including reduced ANT activity) can extend lifespan in C. elegans. The model acknowledged this possibility but then dismissed it in favor of the pro-longevity interpretation, citing loss-of-function phenotypes in other organisms. The model's confidence of 0.62 is moderate but still wrong. The mechanistic reasoning is partially correct in describing the biochemistry but fails to correctly apply the C. elegans-specific context where reduced mitochondrial efficiency often extends lifespan.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}