RGT2
S. cerevisiae
glucose sensor
What the model saw
Gene: RGT2 Organism: Saccharomyces cerevisiae Known functions: glucose sensor. D-glucose binding. carbohydrate:proton symporter activity. transmembrane transporter activity.
View unredacted entry
glucose sensor. D-glucose binding. carbohydrate:proton symporter activity. transmembrane transporter activity.
Solver output
RGT2 is a plasma membrane glucose sensor in S. cerevisiae that detects extracellular glucose and initiates signaling through the Snf3/Rgt2 pathway, ultimately activating expression of hexose transporters (HXT genes) and promoting glucose uptake and utilization. High glucose sensing via RGT2 activates glucose-dependent signaling (including PKA/cAMP and TOR pathways), which suppresses stress response programs, autophagy, and longevity-promoting transcription factors such as Msn2/Msn4 and Rim15. Enhanced glucose sensing and uptake accelerates fermentative metabolism and growth at the expense of mitochondrial respiration, a state associated with shortened chronological and replicative lifespan in yeast. Because RGT2 promotes nutrient-sensing signaling in the presence of glucose—a condition well-established to shorten yeast lifespan—its normal function is predicted to oppose longevity, analogous to the anti-longevity role of upstream nutrient sensors in the TOR/PKA axis.
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 anti_longevity for RGT2. The mechanistic reasoning is sound and well-articulated: RGT2 as a glucose sensor promotes nutrient-sensing signaling that suppresses stress responses and longevity-promoting pathways (Msn2/Msn4, autophagy, mitochondrial respiration). The connection to PKA/cAMP and TOR pathways is reasonable, though RGT2's primary role is in the Snf3/Rgt2 pathway activating HXT gene expression rather than directly activating PKA/TOR. The model appropriately notes this is analogous to other anti-longevity nutrient sensors. The reasoning is largely correct but slightly overstates the direct connection between RGT2 and PKA/TOR pathways — these are downstream effects rather than direct RGT2 signaling. Overall a strong, well-reasoned prediction with appropriate confidence (0.72).
Raw API responses
solver
{
"reasoning": "RGT2 is a plasma membrane glucose sensor in S. cerevisiae that detects extracellular glucose and initiates signaling through the Snf3/Rgt2 pathway, ultimately activating expression of hexose transporters (HXT genes) and promoting glucose uptake and utilization. High glucose sensing via RGT2 activates glucose-dependent signaling (including PKA/cAMP and TOR pathways), which suppresses stress response programs, autophagy, and longevity-promoting transcription factors such as Msn2/Msn4 and Rim15. Enhanced glucose sensing and uptake accelerates fermentative metabolism and growth at the expense of mitochondrial respiration, a state associated with shortened chronological and replicative lifespan in yeast. Because RGT2 promotes nutrient-sensing signaling in the presence of glucose—a condition well-established to shorten yeast lifespan—its normal function is predicted to oppose longevity, analogous to the anti-longevity role of upstream nutrient sensors in the TOR/PKA axis.",
"confidence": 0.72,
"key_pathways": [
"Snf3/Rgt2 glucose sensing pathway",
"PKA/cAMP nutrient signaling",
"TOR pathway / Msn2-Msn4 stress response suppression"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for RGT2. The mechanistic reasoning is sound and well-articulated: RGT2 as a glucose sensor promotes nutrient-sensing signaling that suppresses stress responses and longevity-promoting pathways (Msn2/Msn4, autophagy, mitochondrial respiration). The connection to PKA/cAMP and TOR pathways is reasonable, though RGT2's primary role is in the Snf3/Rgt2 pathway activating HXT gene expression rather than directly activating PKA/TOR. The model appropriately notes this is analogous to other anti-longevity nutrient sensors. The reasoning is largely correct but slightly overstates the direct connection between RGT2 and PKA/TOR pathways — these are downstream effects rather than direct RGT2 signaling. Overall a strong, well-reasoned prediction with appropriate confidence (0.72).",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}