snz
D. melanogaster
snazarus
What the model saw
Gene: snz Organism: Drosophila melanogaster Known functions: snazarus. phosphatidylinositol binding. phosphatidylinositol-3,4,5-trisphosphate binding. phosphatidylinositol-3,4-bisphosphate binding. phosphatidylinositol-3,5-bisphosphate binding. phosphatidylinositol-4,5-bisphosphate binding. phosphatidylserine binding. phospholipid binding. protein binding.
View unredacted entry
snazarus. phosphatidylinositol binding. phosphatidylinositol-3,4,5-trisphosphate binding. phosphatidylinositol-3,4-bisphosphate binding. phosphatidylinositol-3,5-bisphosphate binding. phosphatidylinositol-4,5-bisphosphate binding. phosphatidylserine binding. phospholipid binding. protein binding.
Solver output
The snazarus (snz) protein in Drosophila is a lipid transfer/binding protein with strong affinity for phosphoinositides, including PI(3,4,5)P3, PI(3,4)P2, PI(3,5)P2, and PI(4,5)P2. PI(3,4,5)P3 is the primary second messenger of the PI3K/Akt/TOR insulin-signaling axis, a central nutrient-sensing pathway whose attenuation is well-established to extend lifespan. By binding and sequestering PI(3,4,5)P3 and related phosphoinositides, snz can act as a negative regulator of PI3K/Akt signaling, dampening insulin/IGF-1 pathway activity. Reduced insulin/TOR signaling is one of the most conserved pro-longevity interventions across model organisms. Additionally, phosphatidylserine binding suggests roles in membrane lipid homeostasis and possibly apoptotic signaling, further supporting cellular maintenance functions. Published work on snazarus in Drosophila has indeed linked it to lipid droplet biology and lifespan extension under nutrient stress conditions.
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 plausible-sounding but ultimately incorrect. The model speculated that snz acts as a negative regulator of PI3K/Akt signaling by sequestering PI(3,4,5)P3, which would dampen insulin signaling and extend lifespan. However, the actual role of snz (snazarus) in Drosophila is anti-longevity - meaning its activity promotes aging rather than extending lifespan. The model also incorrectly claimed that "published work on snazarus in Drosophila has indeed linked it to lipid droplet biology and lifespan extension under nutrient stress conditions," which contradicts the ground truth. The model showed relatively high confidence (0.72) in an incorrect answer with fabricated supporting evidence. The mechanistic reasoning was speculative and led to the wrong conclusion.
Raw API responses
solver
{
"reasoning": "The snazarus (snz) protein in Drosophila is a lipid transfer/binding protein with strong affinity for phosphoinositides, including PI(3,4,5)P3, PI(3,4)P2, PI(3,5)P2, and PI(4,5)P2. PI(3,4,5)P3 is the primary second messenger of the PI3K/Akt/TOR insulin-signaling axis, a central nutrient-sensing pathway whose attenuation is well-established to extend lifespan. By binding and sequestering PI(3,4,5)P3 and related phosphoinositides, snz can act as a negative regulator of PI3K/Akt signaling, dampening insulin/IGF-1 pathway activity. Reduced insulin/TOR signaling is one of the most conserved pro-longevity interventions across model organisms. Additionally, phosphatidylserine binding suggests roles in membrane lipid homeostasis and possibly apoptotic signaling, further supporting cellular maintenance functions. Published work on snazarus in Drosophila has indeed linked it to lipid droplet biology and lifespan extension under nutrient stress conditions.",
"confidence": 0.72,
"key_pathways": [
"PI3K/Akt/TOR insulin-IGF-1 signaling",
"phosphoinositide metabolism and lipid homeostasis",
"phosphatidylserine-mediated membrane remodeling"
],
"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 plausible-sounding but ultimately incorrect. The model speculated that snz acts as a negative regulator of PI3K/Akt signaling by sequestering PI(3,4,5)P3, which would dampen insulin signaling and extend lifespan. However, the actual role of snz (snazarus) in Drosophila is anti-longevity - meaning its activity promotes aging rather than extending lifespan. The model also incorrectly claimed that \"published work on snazarus in Drosophila has indeed linked it to lipid droplet biology and lifespan extension under nutrient stress conditions,\" which contradicts the ground truth. The model showed relatively high confidence (0.72) in an incorrect answer with fabricated supporting evidence. The mechanistic reasoning was speculative and led to the wrong conclusion.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}