gig
D. melanogaster
gigas
What the model saw
Gene: gig Organism: Drosophila melanogaster Known functions: gigas. GTPase activator activity. kinase binding. protein binding.
View unredacted entry
gigas. GTPase activator activity. kinase binding. protein binding.
Solver output
The gene *gigas* (gig) in Drosophila encodes the ortholog of the mammalian TSC2 (tuberin), a core component of the TSC1/TSC2 tumor suppressor complex. Its GTPase activator activity is directed toward Rheb (Ras homolog enriched in brain), converting Rheb-GTP to Rheb-GDP and thereby inhibiting TORC1 (Target of Rapamycin Complex 1) signaling. By suppressing TORC1, gig/TSC2 downregulates anabolic processes including protein synthesis and cell growth, and promotes autophagy — all of which are associated with extended lifespan. Loss of gig leads to constitutive TORC1 activation, overgrowth (the "gigas" phenotype), and is expected to shorten lifespan, while normal gig function restrains TOR-driven nutrient sensing and promotes longevity. The kinase binding annotation is consistent with its known interaction with TOR pathway kinases and upstream regulators such as Akt.
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 gig as pro_longevity with high confidence (0.72). The mechanistic reasoning is excellent: correctly identifies gig as the Drosophila TSC2 ortholog, explains its GTPase activator activity toward Rheb, its role in suppressing TORC1, and how this connects to longevity through reduced anabolic signaling and promoted autophagy. The mechanism class "deregulated_nutrient_sensing" is appropriate. All key pathways identified are accurate and relevant.
Raw API responses
solver
{
"reasoning": "The gene *gigas* (gig) in Drosophila encodes the ortholog of the mammalian TSC2 (tuberin), a core component of the TSC1/TSC2 tumor suppressor complex. Its GTPase activator activity is directed toward Rheb (Ras homolog enriched in brain), converting Rheb-GTP to Rheb-GDP and thereby inhibiting TORC1 (Target of Rapamycin Complex 1) signaling. By suppressing TORC1, gig/TSC2 downregulates anabolic processes including protein synthesis and cell growth, and promotes autophagy — all of which are associated with extended lifespan. Loss of gig leads to constitutive TORC1 activation, overgrowth (the \"gigas\" phenotype), and is expected to shorten lifespan, while normal gig function restrains TOR-driven nutrient sensing and promotes longevity. The kinase binding annotation is consistent with its known interaction with TOR pathway kinases and upstream regulators such as Akt.",
"confidence": 0.72,
"key_pathways": [
"TOR/TORC1 signaling (Rheb GTPase activation)",
"TSC1/TSC2 tumor suppressor complex",
"Autophagy induction via TORC1 inhibition"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly identified gig as pro_longevity with high confidence (0.72). The mechanistic reasoning is excellent: correctly identifies gig as the Drosophila TSC2 ortholog, explains its GTPase activator activity toward Rheb, its role in suppressing TORC1, and how this connects to longevity through reduced anabolic signaling and promoted autophagy. The mechanism class \"deregulated_nutrient_sensing\" is appropriate. All key pathways identified are accurate and relevant.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}