bec-1
C. elegans
Beclin homolog
What the model saw
Gene: bec-1 Organism: Caenorhabditis elegans Known functions: Beclin homolog. phosphatidylinositol 3-kinase binding. protein binding. protein-macromolecule adaptor activity.
View unredacted entry
Beclin homolog. phosphatidylinositol 3-kinase binding. protein binding. protein-macromolecule adaptor activity.
Solver output
bec-1 is the C. elegans ortholog of mammalian Beclin-1 (BECN1), a core component of the class III phosphatidylinositol 3-kinase (PI3K) complex (VPS34 complex) that initiates autophagosome nucleation. Its PI3K-binding and protein-macromolecule adaptor activities reflect its role in recruiting the VPS34/PI3K complex to the phagophore assembly site, generating phosphatidylinositol 3-phosphate (PI3P) required for autophagy initiation. Functional macroautophagy is essential for proteostasis maintenance and is required for lifespan extension in multiple C. elegans longevity pathways, including daf-2/insulin signaling reduction and dietary restriction. Loss of bec-1 in C. elegans suppresses longevity in daf-2 mutants and other long-lived strains, demonstrating that its normal function is required for pro-longevity autophagy flux. Therefore, bec-1's normal function promotes longevity by enabling autophagic clearance of damaged proteins and organelles.
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 bec-1 as pro_longevity with high confidence (0.88). The mechanistic reasoning is excellent: it correctly identifies bec-1 as the C. elegans Beclin-1 ortholog, explains its role in autophagosome nucleation via the VPS34/PI3K complex, and correctly notes that loss of bec-1 suppresses longevity in daf-2 mutants and other long-lived strains. The key pathways identified are all relevant and accurate. The reasoning is well-grounded in established C. elegans aging biology.
Raw API responses
solver
{
"reasoning": "bec-1 is the C. elegans ortholog of mammalian Beclin-1 (BECN1), a core component of the class III phosphatidylinositol 3-kinase (PI3K) complex (VPS34 complex) that initiates autophagosome nucleation. Its PI3K-binding and protein-macromolecule adaptor activities reflect its role in recruiting the VPS34/PI3K complex to the phagophore assembly site, generating phosphatidylinositol 3-phosphate (PI3P) required for autophagy initiation. Functional macroautophagy is essential for proteostasis maintenance and is required for lifespan extension in multiple C. elegans longevity pathways, including daf-2/insulin signaling reduction and dietary restriction. Loss of bec-1 in C. elegans suppresses longevity in daf-2 mutants and other long-lived strains, demonstrating that its normal function is required for pro-longevity autophagy flux. Therefore, bec-1's normal function promotes longevity by enabling autophagic clearance of damaged proteins and organelles.",
"confidence": 0.88,
"key_pathways": [
"macroautophagy / autophagosome nucleation (VPS34-Beclin PI3K complex)",
"daf-2/insulin-IGF-1 signaling longevity pathway",
"proteostasis maintenance via autophagic flux"
],
"mechanism_class": "disabled_macroautophagy",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identified bec-1 as pro_longevity with high confidence (0.88). The mechanistic reasoning is excellent: it correctly identifies bec-1 as the C. elegans Beclin-1 ortholog, explains its role in autophagosome nucleation via the VPS34/PI3K complex, and correctly notes that loss of bec-1 suppresses longevity in daf-2 mutants and other long-lived strains. The key pathways identified are all relevant and accurate. The reasoning is well-grounded in established C. elegans aging biology.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}