ght5
S. pombe
plasma membrane high-affinity glucose/fructose:proton symporter Ght5
What the model saw
Gene: ght5 Organism: Schizosaccharomyces pombe Known functions: plasma membrane high-affinity glucose/fructose:proton symporter Ght5. carbohydrate:proton symporter activity. high-affinity D-glucose transmembrane transporter activity. transmembrane transporter activity.
View unredacted entry
plasma membrane high-affinity glucose/fructose:proton symporter Ght5. carbohydrate:proton symporter activity. high-affinity D-glucose transmembrane transporter activity. transmembrane transporter activity.
Solver output
Ght5 is a high-affinity glucose/fructose:proton symporter at the plasma membrane, responsible for importing glucose under low-glucose conditions in S. pombe. High-affinity glucose transporters are typically upregulated when glucose is scarce, enabling cells to maintain minimal but sufficient glucose uptake under caloric restriction-like conditions. By facilitating efficient glucose sensing and import at low concentrations, Ght5 supports the cell's ability to adapt to nutrient-limited environments, which is associated with reduced PKA/TOR signaling and extended lifespan. This places Ght5 within the deregulated nutrient-sensing hallmark, as glucose transporter activity directly feeds into glucose-dependent signaling cascades (cAMP-PKA, TORC1) that regulate longevity. Loss of high-affinity transporters would impair the cell's ability to respond appropriately to low-glucose conditions, potentially dysregulating nutrient sensing and shortening 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 plausible on the surface but ultimately incorrect. It argues that Ght5 supports caloric restriction-like conditions by enabling efficient glucose uptake at low concentrations, which would extend lifespan. However, the actual effect is anti-longevity. In reality, a high-affinity glucose transporter like Ght5 would promote glucose uptake and thus activate pro-aging nutrient sensing pathways (PKA, TORC1) even under low-glucose conditions — the opposite of what caloric restriction achieves. The model's logic is internally inconsistent: it correctly identifies that glucose import feeds into PKA/TOR signaling but then incorrectly concludes this would be pro-longevity. Loss of Ght5 would more likely mimic caloric restriction by reducing glucose signaling, which would extend lifespan — making Ght5 itself anti-longevity. The model had moderate confidence (0.62) but reached the wrong conclusion with flawed mechanistic reasoning.
Raw API responses
solver
{
"reasoning": "Ght5 is a high-affinity glucose/fructose:proton symporter at the plasma membrane, responsible for importing glucose under low-glucose conditions in S. pombe. High-affinity glucose transporters are typically upregulated when glucose is scarce, enabling cells to maintain minimal but sufficient glucose uptake under caloric restriction-like conditions. By facilitating efficient glucose sensing and import at low concentrations, Ght5 supports the cell's ability to adapt to nutrient-limited environments, which is associated with reduced PKA/TOR signaling and extended lifespan. This places Ght5 within the deregulated nutrient-sensing hallmark, as glucose transporter activity directly feeds into glucose-dependent signaling cascades (cAMP-PKA, TORC1) that regulate longevity. Loss of high-affinity transporters would impair the cell's ability to respond appropriately to low-glucose conditions, potentially dysregulating nutrient sensing and shortening lifespan.",
"confidence": 0.62,
"key_pathways": [
"high-affinity glucose transport",
"cAMP-PKA nutrient sensing",
"TORC1 signaling"
],
"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 on the surface but ultimately incorrect. It argues that Ght5 supports caloric restriction-like conditions by enabling efficient glucose uptake at low concentrations, which would extend lifespan. However, the actual effect is anti-longevity. In reality, a high-affinity glucose transporter like Ght5 would promote glucose uptake and thus activate pro-aging nutrient sensing pathways (PKA, TORC1) even under low-glucose conditions — the opposite of what caloric restriction achieves. The model's logic is internally inconsistent: it correctly identifies that glucose import feeds into PKA/TOR signaling but then incorrectly concludes this would be pro-longevity. Loss of Ght5 would more likely mimic caloric restriction by reducing glucose signaling, which would extend lifespan — making Ght5 itself anti-longevity. The model had moderate confidence (0.62) but reached the wrong conclusion with flawed mechanistic reasoning.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}