DNM1
S. cerevisiae
dynamin-related GTPase DNM1
What the model saw
Gene: DNM1 Organism: Saccharomyces cerevisiae Known functions: dynamin-related GTPase DNM1. GTP binding. GTPase activity. identical protein binding. microtubule binding.
View unredacted entry
dynamin-related GTPase DNM1. GTP binding. GTPase activity. identical protein binding. microtubule binding.
Solver output
DNM1 encodes the yeast dynamin-related GTPase that is the master regulator of mitochondrial fission. Its GTPase activity drives the scission of the outer mitochondrial membrane, fragmenting the mitochondrial network. Excessive mitochondrial fission driven by DNM1 is associated with mitochondrial dysfunction, loss of membrane potential, and increased reactive oxygen species production. In yeast aging studies, deletion of DNM1 shifts the mitochondrial network toward fusion, which is associated with extended chronological and replicative lifespan, indicating that DNM1's normal pro-fission activity is detrimental to longevity. The identical protein binding annotation is consistent with DNM1's known self-assembly into oligomeric ring structures required for membrane constriction and fission execution.
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 correctly identified DNM1 as anti_longevity with high confidence (0.82). The mechanistic reasoning is excellent and accurate: DNM1 is indeed the yeast ortholog of dynamin-related GTPase that drives mitochondrial fission, and deletion of DNM1 shifts the balance toward mitochondrial fusion, which extends lifespan in yeast. The model correctly connects the GTPase activity annotation to mitochondrial fission, explains the self-assembly via identical protein binding, and accurately describes the downstream consequences (ROS, membrane potential loss). The key pathways identified are all relevant and correct.
Raw API responses
solver
{
"reasoning": "DNM1 encodes the yeast dynamin-related GTPase that is the master regulator of mitochondrial fission. Its GTPase activity drives the scission of the outer mitochondrial membrane, fragmenting the mitochondrial network. Excessive mitochondrial fission driven by DNM1 is associated with mitochondrial dysfunction, loss of membrane potential, and increased reactive oxygen species production. In yeast aging studies, deletion of DNM1 shifts the mitochondrial network toward fusion, which is associated with extended chronological and replicative lifespan, indicating that DNM1's normal pro-fission activity is detrimental to longevity. The identical protein binding annotation is consistent with DNM1's known self-assembly into oligomeric ring structures required for membrane constriction and fission execution.",
"confidence": 0.82,
"key_pathways": [
"mitochondrial fission",
"dynamin GTPase-mediated membrane scission",
"mitochondrial network dynamics"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified DNM1 as anti_longevity with high confidence (0.82). The mechanistic reasoning is excellent and accurate: DNM1 is indeed the yeast ortholog of dynamin-related GTPase that drives mitochondrial fission, and deletion of DNM1 shifts the balance toward mitochondrial fusion, which extends lifespan in yeast. The model correctly connects the GTPase activity annotation to mitochondrial fission, explains the self-assembly via identical protein binding, and accurately describes the downstream consequences (ROS, membrane potential loss). The key pathways identified are all relevant and correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}