lgg-1
C. elegans
Protein lgg-1
What the model saw
Gene: lgg-1 Organism: Caenorhabditis elegans Known functions: Protein lgg-1. GABA receptor binding. phosphatidylethanolamine binding. protein binding. ubiquitin protein ligase binding.
View unredacted entry
Protein lgg-1. GABA receptor binding. phosphatidylethanolamine binding. protein binding. ubiquitin protein ligase binding.
Solver output
lgg-1 is the C. elegans ortholog of mammalian LC3/GABARAP, a central effector of macroautophagy. Its phosphatidylethanolamine (PE) binding activity reflects the lipidation step (LC3-I to LC3-II conversion) that is essential for autophagosome membrane elongation and closure. Its ubiquitin protein ligase binding supports selective autophagy cargo recognition via autophagy receptors. PE-conjugated LGG-1 is recruited to the phagophore and drives autophagosome biogenesis, a process required for clearance of damaged proteins and organelles. Robust autophagy flux through LGG-1 is well-established to extend lifespan in C. elegans, acting downstream of multiple longevity pathways including DAF-16/FOXO, TOR inhibition, and dietary restriction.
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 lgg-1 as pro_longevity with high confidence (0.92). The mechanistic reasoning is excellent: it correctly identifies LGG-1 as the C. elegans LC3/GABARAP ortholog, explains the PE-lipidation step (LC3-I to LC3-II conversion) for autophagosome biogenesis, and correctly links robust autophagy flux to lifespan extension downstream of DAF-16/FOXO, TOR inhibition, and dietary restriction pathways. The mechanism_class label "disabled_macroautophagy" is slightly confusing (it seems to describe what happens when lgg-1 is lost rather than what lgg-1 does), but the textual reasoning is fully correct and coherent. All key pathways cited are accurate and well-supported by the literature.
Raw API responses
solver
{
"reasoning": "lgg-1 is the C. elegans ortholog of mammalian LC3/GABARAP, a central effector of macroautophagy. Its phosphatidylethanolamine (PE) binding activity reflects the lipidation step (LC3-I to LC3-II conversion) that is essential for autophagosome membrane elongation and closure. Its ubiquitin protein ligase binding supports selective autophagy cargo recognition via autophagy receptors. PE-conjugated LGG-1 is recruited to the phagophore and drives autophagosome biogenesis, a process required for clearance of damaged proteins and organelles. Robust autophagy flux through LGG-1 is well-established to extend lifespan in C. elegans, acting downstream of multiple longevity pathways including DAF-16/FOXO, TOR inhibition, and dietary restriction.",
"confidence": 0.92,
"key_pathways": [
"macroautophagy / autophagosome biogenesis (LC3/LGG-1 lipidation)",
"TOR signaling and dietary restriction longevity axis",
"selective autophagy via ubiquitin-receptor interactions"
],
"mechanism_class": "disabled_macroautophagy",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identified lgg-1 as pro_longevity with high confidence (0.92). The mechanistic reasoning is excellent: it correctly identifies LGG-1 as the C. elegans LC3/GABARAP ortholog, explains the PE-lipidation step (LC3-I to LC3-II conversion) for autophagosome biogenesis, and correctly links robust autophagy flux to lifespan extension downstream of DAF-16/FOXO, TOR inhibition, and dietary restriction pathways. The mechanism_class label \"disabled_macroautophagy\" is slightly confusing (it seems to describe what happens when lgg-1 is lost rather than what lgg-1 does), but the textual reasoning is fully correct and coherent. All key pathways cited are accurate and well-supported by the literature.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}