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nuo-1

C. elegans

NADH dehydrogenase

What the model saw

Gene: nuo-1
Organism: Caenorhabditis elegans
Known functions: NADH dehydrogenase. 4 iron, 4 sulfur cluster binding. FMN binding. NAD binding. NADH dehydrogenase (ubiquinone) activity.
View unredacted entry
NADH dehydrogenase. 4 iron, 4 sulfur cluster binding. FMN binding. NAD binding. NADH dehydrogenase (ubiquinone) activity.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Mitochondrial dysfunction
Reasoning

nuo-1 encodes the 51 kDa flavoprotein subunit of mitochondrial Complex I (NADH:ubiquinone oxidoreductase), the entry point for electrons from NADH into the electron transport chain. Its FMN-binding and 4Fe-4S cluster-binding activities are essential for electron transfer from NADH to ubiquinone. In C. elegans, partial loss-of-function of Complex I subunits (e.g., via RNAi) is well-documented to extend lifespan, consistent with the mitohormesis model where mild mitochondrial electron transport chain impairment reduces ROS production at Complex I and/or activates compensatory stress-response pathways (HIF-1, DAF-16). Full wild-type activity of nuo-1 therefore sustains maximal Complex I flux, which is associated with higher mitochondrial ROS output and shorter lifespan, making the normal function of this gene anti-longevity. The NAD-binding activity also links Complex I to the NAD⁺/NADH ratio, a key regulator of sirtuin activity and metabolic aging.

Key pathways
Mitochondrial Complex I / electron transport chainMitohormesis / ROS signalingNAD+/NADH redox balance
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
5/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for nuo-1. The mechanistic reasoning is excellent: it correctly identifies nuo-1 as the 51 kDa flavoprotein subunit of Complex I, explains the FMN and 4Fe-4S cluster roles in electron transfer, and correctly invokes the mitohormesis model where partial loss-of-function of Complex I subunits extends lifespan in C. elegans (meaning wild-type function is anti-longevity). The model also correctly notes the NAD+/NADH ratio connection. The confidence level of 0.72 is appropriate given the complexity of the relationship. All key pathways identified are relevant and accurate.

Raw API responses

solver

{
  "reasoning": "nuo-1 encodes the 51 kDa flavoprotein subunit of mitochondrial Complex I (NADH:ubiquinone oxidoreductase), the entry point for electrons from NADH into the electron transport chain. Its FMN-binding and 4Fe-4S cluster-binding activities are essential for electron transfer from NADH to ubiquinone. In C. elegans, partial loss-of-function of Complex I subunits (e.g., via RNAi) is well-documented to extend lifespan, consistent with the mitohormesis model where mild mitochondrial electron transport chain impairment reduces ROS production at Complex I and/or activates compensatory stress-response pathways (HIF-1, DAF-16). Full wild-type activity of nuo-1 therefore sustains maximal Complex I flux, which is associated with higher mitochondrial ROS output and shorter lifespan, making the normal function of this gene anti-longevity. The NAD-binding activity also links Complex I to the NAD⁺/NADH ratio, a key regulator of sirtuin activity and metabolic aging.",
  "confidence": 0.72,
  "key_pathways": [
    "Mitochondrial Complex I / electron transport chain",
    "Mitohormesis / ROS signaling",
    "NAD+/NADH redox balance"
  ],
  "mechanism_class": "mitochondrial_dysfunction",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for nuo-1. The mechanistic reasoning is excellent: it correctly identifies nuo-1 as the 51 kDa flavoprotein subunit of Complex I, explains the FMN and 4Fe-4S cluster roles in electron transfer, and correctly invokes the mitohormesis model where partial loss-of-function of Complex I subunits extends lifespan in C. elegans (meaning wild-type function is anti-longevity). The model also correctly notes the NAD+/NADH ratio connection. The confidence level of 0.72 is appropriate given the complexity of the relationship. All key pathways identified are relevant and accurate.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}