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Glyp

D. melanogaster

Glycogen phosphorylase

What the model saw

Gene: Glyp
Organism: Drosophila melanogaster
Known functions: Glycogen phosphorylase. glycogen phosphorylase. 1,4-alpha-oligoglucan phosphorylase activity. glycogen phosphorylase activity. protein homodimerization activity. pyridoxal phosphate binding.
View unredacted entry
Glycogen phosphorylase. glycogen phosphorylase. 1,4-alpha-oligoglucan phosphorylase activity. glycogen phosphorylase activity. protein homodimerization activity. pyridoxal phosphate binding.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

Glycogen phosphorylase (Glyp) catalyzes the rate-limiting step of glycogenolysis, cleaving glucose-1-phosphate from glycogen to mobilize stored glucose. Elevated glycogen phosphorylase activity increases circulating glucose and feeds into glycolytic and insulin/IGF-1 signaling pathways. In Drosophila, hyperactivation of nutrient-sensing pathways (IIS/TOR) is well-established to shorten lifespan, and excessive glucose mobilization would promote anabolic signaling and suppress FOXO-mediated pro-longevity transcription. Additionally, increased glycolytic flux can elevate reactive oxygen species production via mitochondrial respiration, contributing to oxidative stress. Loss-of-function or reduced activity of glycogen phosphorylase would be expected to conserve glycogen stores, dampen IIS/TOR signaling, and extend lifespan, consistent with the pro-longevity effects of dietary restriction and reduced glucose availability observed in flies.

Key pathways
insulin/IGF-1 signaling (IIS) / FOXO pathwayglycogenolysis / glucose mobilizationTOR nutrient-sensing pathway
Longevity influence
Anti-longevity
Lifespan effect
Increase

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

Answer
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for Glyp (glycogen phosphorylase) in Drosophila. The mechanistic reasoning is biologically coherent: glycogen phosphorylase mobilizes glucose, which can feed into IIS/TOR signaling and promote anabolic pathways that shorten lifespan. The reasoning about reduced Glyp activity conserving glycogen and dampening nutrient-sensing pathways is plausible. The model appropriately connects glycogenolysis to known longevity-relevant pathways. Confidence of 0.72 is reasonable. The reasoning is somewhat speculative (connecting glycogen mobilization to IIS/TOR) but is mechanistically sound and consistent with known biology in Drosophila.

Raw API responses

solver

{
  "reasoning": "Glycogen phosphorylase (Glyp) catalyzes the rate-limiting step of glycogenolysis, cleaving glucose-1-phosphate from glycogen to mobilize stored glucose. Elevated glycogen phosphorylase activity increases circulating glucose and feeds into glycolytic and insulin/IGF-1 signaling pathways. In Drosophila, hyperactivation of nutrient-sensing pathways (IIS/TOR) is well-established to shorten lifespan, and excessive glucose mobilization would promote anabolic signaling and suppress FOXO-mediated pro-longevity transcription. Additionally, increased glycolytic flux can elevate reactive oxygen species production via mitochondrial respiration, contributing to oxidative stress. Loss-of-function or reduced activity of glycogen phosphorylase would be expected to conserve glycogen stores, dampen IIS/TOR signaling, and extend lifespan, consistent with the pro-longevity effects of dietary restriction and reduced glucose availability observed in flies.",
  "confidence": 0.72,
  "key_pathways": [
    "insulin/IGF-1 signaling (IIS) / FOXO pathway",
    "glycogenolysis / glucose mobilization",
    "TOR nutrient-sensing pathway"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for Glyp (glycogen phosphorylase) in Drosophila. The mechanistic reasoning is biologically coherent: glycogen phosphorylase mobilizes glucose, which can feed into IIS/TOR signaling and promote anabolic pathways that shorten lifespan. The reasoning about reduced Glyp activity conserving glycogen and dampening nutrient-sensing pathways is plausible. The model appropriately connects glycogenolysis to known longevity-relevant pathways. Confidence of 0.72 is reasonable. The reasoning is somewhat speculative (connecting glycogen mobilization to IIS/TOR) but is mechanistically sound and consistent with known biology in Drosophila.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}