← Browse entries

park

D. melanogaster

parkin

What the model saw

Gene: park
Organism: Drosophila melanogaster
Known functions: parkin. protein binding. ubiquitin conjugating enzyme binding. ubiquitin protein ligase activity. ubiquitin-protein transferase activity. zinc ion binding.
View unredacted entry
parkin. protein binding. ubiquitin conjugating enzyme binding. ubiquitin protein ligase activity. ubiquitin-protein transferase activity. zinc ion binding.

Solver output

Predicted influence
Pro-longevity
Confidence
82%
Mechanism
Mitochondrial dysfunction
Reasoning

Park (Drosophila parkin) is an E3 ubiquitin-protein ligase that is the central effector of PINK1/Parkin-mediated mitophagy, the selective autophagic clearance of damaged mitochondria. By ubiquitinating outer mitochondrial membrane proteins (e.g., Mfn/Marf, VDAC), Parkin targets dysfunctional mitochondria for degradation, thereby maintaining a healthy mitochondrial pool and preventing accumulation of ROS-generating, depolarized organelles. Loss of park in Drosophila leads to mitochondrial dysfunction, muscle degeneration, and reduced lifespan, while its normal function suppresses age-associated mitochondrial deterioration. This places park squarely within the mitochondrial quality-control axis of the mitochondrial dysfunction hallmark of aging. Its ubiquitin ligase and zinc-binding (RING domain) activities are the molecular basis for substrate recognition and ubiquitin transfer in this pathway.

Key pathways
PINK1/Parkin mitophagyubiquitin-proteasome systemmitochondrial quality control
Longevity influence
Pro-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
5/5
Failure mode
Correct
Notes

The model correctly predicted pro_longevity for Drosophila park (parkin). The mechanistic reasoning is excellent and accurate: park encodes an E3 ubiquitin-protein ligase that functions in PINK1/Parkin-mediated mitophagy, maintaining mitochondrial quality. Loss of park leads to mitochondrial dysfunction and reduced lifespan, while normal function is pro-longevity. The model correctly identifies the RING domain zinc-binding activity as the molecular basis for ubiquitin transfer, and correctly names key substrates (Mfn/Marf, VDAC). The confidence level of 0.82 is appropriate given the well-established literature on this gene.

Raw API responses

solver

{
  "reasoning": "Park (Drosophila parkin) is an E3 ubiquitin-protein ligase that is the central effector of PINK1/Parkin-mediated mitophagy, the selective autophagic clearance of damaged mitochondria. By ubiquitinating outer mitochondrial membrane proteins (e.g., Mfn/Marf, VDAC), Parkin targets dysfunctional mitochondria for degradation, thereby maintaining a healthy mitochondrial pool and preventing accumulation of ROS-generating, depolarized organelles. Loss of park in Drosophila leads to mitochondrial dysfunction, muscle degeneration, and reduced lifespan, while its normal function suppresses age-associated mitochondrial deterioration. This places park squarely within the mitochondrial quality-control axis of the mitochondrial dysfunction hallmark of aging. Its ubiquitin ligase and zinc-binding (RING domain) activities are the molecular basis for substrate recognition and ubiquitin transfer in this pathway.",
  "confidence": 0.82,
  "key_pathways": [
    "PINK1/Parkin mitophagy",
    "ubiquitin-proteasome system",
    "mitochondrial quality control"
  ],
  "mechanism_class": "mitochondrial_dysfunction",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for Drosophila park (parkin). The mechanistic reasoning is excellent and accurate: park encodes an E3 ubiquitin-protein ligase that functions in PINK1/Parkin-mediated mitophagy, maintaining mitochondrial quality. Loss of park leads to mitochondrial dysfunction and reduced lifespan, while normal function is pro-longevity. The model correctly identifies the RING domain zinc-binding activity as the molecular basis for ubiquitin transfer, and correctly names key substrates (Mfn/Marf, VDAC). The confidence level of 0.82 is appropriate given the well-established literature on this gene.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}