unc-10
C. elegans
Rab-3-interacting molecule unc-10
What the model saw
Gene: unc-10 Organism: Caenorhabditis elegans Known functions: Rab-3-interacting molecule unc-10. protein binding. small GTPase binding. structural constituent of presynaptic active zone.
View unredacted entry
Rab-3-interacting molecule unc-10. protein binding. small GTPase binding. structural constituent of presynaptic active zone.
Solver output
UNC-10 is the C. elegans ortholog of RIM1/RIM2 (Rab3-interacting molecules), functioning as a structural scaffold of the presynaptic active zone that coordinates synaptic vesicle docking and priming via interaction with the small GTPase RAB-3. As a core active zone component, UNC-10 promotes efficient neurotransmitter release and synaptic signaling. In C. elegans, enhanced neuronal signaling—particularly through cholinergic and other excitatory pathways—is generally associated with reduced lifespan, while reduced synaptic transmission (e.g., in eat-4 or unc-13 mutants) can extend lifespan. Loss-of-function mutations in active zone scaffolding proteins that dampen neurotransmission have been linked to longevity benefits, suggesting the normal pro-synaptic function of UNC-10 opposes longevity. This fits within the altered intercellular communication hallmark, as synaptic signaling is a primary mode of cell-to-cell communication in the nervous system that influences systemic aging.
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 predicted anti_longevity for unc-10. The mechanistic reasoning is plausible and well-constructed: UNC-10/RIM functions as a presynaptic active zone scaffold promoting neurotransmitter release, and the model correctly reasons that enhanced synaptic signaling tends to reduce lifespan in C. elegans, while loss-of-function in such components can extend lifespan. The mechanism class of "altered_intercellular_communication" is appropriate for a synaptic signaling gene. The reasoning is solid though somewhat speculative (drawing analogies from eat-4 and unc-13 rather than citing direct unc-10 longevity studies), which is reflected in the moderate confidence of 0.62. Overall a well-reasoned correct prediction.
Raw API responses
solver
{
"reasoning": "UNC-10 is the C. elegans ortholog of RIM1/RIM2 (Rab3-interacting molecules), functioning as a structural scaffold of the presynaptic active zone that coordinates synaptic vesicle docking and priming via interaction with the small GTPase RAB-3. As a core active zone component, UNC-10 promotes efficient neurotransmitter release and synaptic signaling. In C. elegans, enhanced neuronal signaling—particularly through cholinergic and other excitatory pathways—is generally associated with reduced lifespan, while reduced synaptic transmission (e.g., in eat-4 or unc-13 mutants) can extend lifespan. Loss-of-function mutations in active zone scaffolding proteins that dampen neurotransmission have been linked to longevity benefits, suggesting the normal pro-synaptic function of UNC-10 opposes longevity. This fits within the altered intercellular communication hallmark, as synaptic signaling is a primary mode of cell-to-cell communication in the nervous system that influences systemic aging.",
"confidence": 0.62,
"key_pathways": [
"presynaptic active zone assembly and vesicle priming",
"RAB-3 GTPase-dependent synaptic vesicle docking",
"neurotransmitter release and intercellular signaling"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for unc-10. The mechanistic reasoning is plausible and well-constructed: UNC-10/RIM functions as a presynaptic active zone scaffold promoting neurotransmitter release, and the model correctly reasons that enhanced synaptic signaling tends to reduce lifespan in C. elegans, while loss-of-function in such components can extend lifespan. The mechanism class of \"altered_intercellular_communication\" is appropriate for a synaptic signaling gene. The reasoning is solid though somewhat speculative (drawing analogies from eat-4 and unc-13 rather than citing direct unc-10 longevity studies), which is reflected in the moderate confidence of 0.62. Overall a well-reasoned correct prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}