egl-30
C. elegans
Guanine nucleotide-binding protein subunit alpha
What the model saw
Gene: egl-30 Organism: Caenorhabditis elegans Known functions: Guanine nucleotide-binding protein subunit alpha. G protein-coupled receptor binding. G-protein beta/gamma-subunit complex binding. GTP binding. GTPase activity. guanyl nucleotide binding. metal ion binding.
View unredacted entry
Guanine nucleotide-binding protein subunit alpha. G protein-coupled receptor binding. G-protein beta/gamma-subunit complex binding. GTP binding. GTPase activity. guanyl nucleotide binding. metal ion binding.
Solver output
egl-30 encodes the C. elegans Gαq homolog, a heterotrimeric G protein alpha subunit that couples GPCRs to downstream effectors including phospholipase C-β (EGL-8) and the Trio/RhoGEF pathway. Activated Gαq signaling stimulates DAG/PKC and IP3 pathways, which broadly promote anabolic and growth-promoting signaling. In C. elegans, enhanced Gαq/egl-30 activity has been shown to antagonize the pro-longevity DAF-16/FOXO transcription factor pathway by promoting insulin-like signaling tone and reducing stress resistance. Conversely, reduction of egl-30 function extends lifespan, consistent with its role as a pro-growth, anti-longevity signal. This places egl-30 in the deregulated nutrient-sensing hallmark, as Gαq-PKC signaling intersects with insulin/IGF-1-like pathway regulation of DAF-16 and metabolic homeostasis.
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 egl-30 as anti_longevity with good confidence (0.72). The mechanistic reasoning is largely accurate: egl-30 encodes the C. elegans Gαq homolog, and its reduction extends lifespan. The model correctly identifies the PLCβ/DAG/IP3 pathway and PKC signaling. The connection to DAF-16/FOXO and insulin-like signaling is plausible but somewhat speculative - the primary mechanism of egl-30's anti-longevity effect is more directly through Gαq-PLCβ signaling and its effects on neuronal activity/feeding behavior rather than strictly through deregulated nutrient sensing. The mechanism_class of "deregulated_nutrient_sensing" is a reasonable but not perfect categorization - Gαq signaling is more of a general GPCR/neuromodulatory pathway. Overall, the answer is correct and the reasoning is solid, though the nutrient sensing framing is a slight overreach.
Raw API responses
solver
{
"reasoning": "egl-30 encodes the C. elegans Gαq homolog, a heterotrimeric G protein alpha subunit that couples GPCRs to downstream effectors including phospholipase C-β (EGL-8) and the Trio/RhoGEF pathway. Activated Gαq signaling stimulates DAG/PKC and IP3 pathways, which broadly promote anabolic and growth-promoting signaling. In C. elegans, enhanced Gαq/egl-30 activity has been shown to antagonize the pro-longevity DAF-16/FOXO transcription factor pathway by promoting insulin-like signaling tone and reducing stress resistance. Conversely, reduction of egl-30 function extends lifespan, consistent with its role as a pro-growth, anti-longevity signal. This places egl-30 in the deregulated nutrient-sensing hallmark, as Gαq-PKC signaling intersects with insulin/IGF-1-like pathway regulation of DAF-16 and metabolic homeostasis.",
"confidence": 0.72,
"key_pathways": [
"Gαq-PLCβ-DAG/IP3 signaling",
"Insulin/IGF-1-like signaling (DAF-2/DAF-16 axis)",
"PKC-mediated anabolic signaling"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted egl-30 as anti_longevity with good confidence (0.72). The mechanistic reasoning is largely accurate: egl-30 encodes the C. elegans Gαq homolog, and its reduction extends lifespan. The model correctly identifies the PLCβ/DAG/IP3 pathway and PKC signaling. The connection to DAF-16/FOXO and insulin-like signaling is plausible but somewhat speculative - the primary mechanism of egl-30's anti-longevity effect is more directly through Gαq-PLCβ signaling and its effects on neuronal activity/feeding behavior rather than strictly through deregulated nutrient sensing. The mechanism_class of \"deregulated_nutrient_sensing\" is a reasonable but not perfect categorization - Gαq signaling is more of a general GPCR/neuromodulatory pathway. Overall, the answer is correct and the reasoning is solid, though the nutrient sensing framing is a slight overreach.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}