gpa-15
C. elegans
Guanine nucleotide-binding protein alpha-15 subunit
What the model saw
Gene: gpa-15 Organism: Caenorhabditis elegans Known functions: Guanine nucleotide-binding protein alpha-15 subunit. G protein-coupled receptor binding. G-protein beta/gamma-subunit complex binding. GTPase activity. guanyl nucleotide binding.
View unredacted entry
Guanine nucleotide-binding protein alpha-15 subunit. G protein-coupled receptor binding. G-protein beta/gamma-subunit complex binding. GTPase activity. guanyl nucleotide binding.
Solver output
gpa-15 encodes a Gα subunit that couples GPCRs to downstream effectors via GTPase cycling. In C. elegans, Gα proteins in sensory neurons (particularly chemosensory GPCRs) modulate the DAF-2/insulin-IGF-1 signaling axis by regulating neuronal release of insulin-like peptides; reduced sensory signaling through this pathway typically promotes DAF-16/FOXO nuclear localization and extends lifespan. gpa-15 is expressed in chemosensory neurons and its activity in GPCR-coupled signaling can influence nutrient-sensing and neuroendocrine outputs that feed into the IIS pathway. Gα subunits with GTPase activity transduce signals that, when active, may promote insulin-like peptide secretion and thus suppress longevity; however, the net effect of Gα signaling in sensory neurons in C. elegans is context-dependent and several Gα subunits have been shown to be pro-longevity when functioning in specific sensory circuits that antagonize IIS. The binding to Gβγ complexes and GPCR coupling places this gene squarely in the neuroendocrine nutrient-sensing axis that is a central regulator of C. elegans lifespan.
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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is generic and speculative about G-alpha subunit function in C. elegans sensory neurons and IIS pathway modulation. While the model acknowledges context-dependence, it ultimately guesses the wrong direction. The mechanistic reasoning about sensory neuron GPCR signaling and IIS is plausible in general terms but doesn't correctly identify gpa-15's actual anti-longevity role. The model's confidence of 0.55 is relatively low, but it still committed to the wrong answer. The reasoning quality is poor because it relies on generic G-protein biology rather than specific knowledge about gpa-15, and the conclusion drawn is incorrect.
Raw API responses
solver
{
"reasoning": "gpa-15 encodes a Gα subunit that couples GPCRs to downstream effectors via GTPase cycling. In C. elegans, Gα proteins in sensory neurons (particularly chemosensory GPCRs) modulate the DAF-2/insulin-IGF-1 signaling axis by regulating neuronal release of insulin-like peptides; reduced sensory signaling through this pathway typically promotes DAF-16/FOXO nuclear localization and extends lifespan. gpa-15 is expressed in chemosensory neurons and its activity in GPCR-coupled signaling can influence nutrient-sensing and neuroendocrine outputs that feed into the IIS pathway. Gα subunits with GTPase activity transduce signals that, when active, may promote insulin-like peptide secretion and thus suppress longevity; however, the net effect of Gα signaling in sensory neurons in C. elegans is context-dependent and several Gα subunits have been shown to be pro-longevity when functioning in specific sensory circuits that antagonize IIS. The binding to Gβγ complexes and GPCR coupling places this gene squarely in the neuroendocrine nutrient-sensing axis that is a central regulator of C. elegans lifespan.",
"confidence": 0.55,
"key_pathways": [
"insulin/IGF-1 signaling (IIS) / DAF-2–DAF-16 axis",
"GPCR-coupled sensory neuron signaling",
"G-protein alpha subunit GTPase cycle"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is generic and speculative about G-alpha subunit function in C. elegans sensory neurons and IIS pathway modulation. While the model acknowledges context-dependence, it ultimately guesses the wrong direction. The mechanistic reasoning about sensory neuron GPCR signaling and IIS is plausible in general terms but doesn't correctly identify gpa-15's actual anti-longevity role. The model's confidence of 0.55 is relatively low, but it still committed to the wrong answer. The reasoning quality is poor because it relies on generic G-protein biology rather than specific knowledge about gpa-15, and the conclusion drawn is incorrect.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}