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MBA1

S. cerevisiae

Mba1p

What the model saw

Gene: MBA1
Organism: Saccharomyces cerevisiae
Known functions: Mba1p. mitochondrial ribosome binding. ribosome binding.
View unredacted entry
Mba1p. mitochondrial ribosome binding. ribosome binding.

Solver output

Predicted influence
Pro-longevity
Confidence
62%
Mechanism
Mitochondrial dysfunction
Reasoning

MBA1 encodes a mitochondrial ribosome receptor (membrane-binding factor) that tethers mitochondrial ribosomes to the inner mitochondrial membrane, facilitating co-translational insertion of mitochondrially-encoded OXPHOS subunits. Proper membrane anchoring of the mitoribosome is essential for efficient synthesis and assembly of respiratory chain complexes. Loss of this function would impair OXPHOS complex assembly, reduce mitochondrial membrane potential, and increase ROS production — all hallmarks of mitochondrial dysfunction that accelerate aging. By supporting robust mitochondrial translation and respiratory chain integrity, MBA1's normal function helps maintain mitochondrial homeostasis, which is strongly associated with longevity in yeast and other organisms.

Key pathways
mitochondrial translationOXPHOS complex assemblymitochondrial ribosome membrane tethering
Longevity influence
Anti-longevity
Lifespan effect
Increase and Decrease

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
Incorrect
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Confident wrong
Notes

The model predicted pro_longevity but the ground truth is anti_longevity. MBA1 is anti-longevity in yeast, meaning its deletion extends lifespan rather than shortening it. The model's reasoning assumes that because MBA1 supports mitochondrial translation and OXPHOS assembly, its loss would be harmful and thus the gene must be pro-longevity. However, this logic is flawed — reduced mitochondrial translation/OXPHOS activity is actually associated with lifespan extension in yeast (similar to how mitochondrial dysfunction can paradoxically extend lifespan through hormesis or reduced ROS production from a less active respiratory chain). The model's mechanistic reasoning about the gene's function is broadly correct (MBA1 tethers mitoribosomes to the inner membrane), but the inference about longevity direction is wrong. The model was moderately confident (0.62) in the wrong direction.

Raw API responses

solver

{
  "reasoning": "MBA1 encodes a mitochondrial ribosome receptor (membrane-binding factor) that tethers mitochondrial ribosomes to the inner mitochondrial membrane, facilitating co-translational insertion of mitochondrially-encoded OXPHOS subunits. Proper membrane anchoring of the mitoribosome is essential for efficient synthesis and assembly of respiratory chain complexes. Loss of this function would impair OXPHOS complex assembly, reduce mitochondrial membrane potential, and increase ROS production — all hallmarks of mitochondrial dysfunction that accelerate aging. By supporting robust mitochondrial translation and respiratory chain integrity, MBA1's normal function helps maintain mitochondrial homeostasis, which is strongly associated with longevity in yeast and other organisms.",
  "confidence": 0.62,
  "key_pathways": [
    "mitochondrial translation",
    "OXPHOS complex assembly",
    "mitochondrial ribosome membrane tethering"
  ],
  "mechanism_class": "mitochondrial_dysfunction",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model predicted pro_longevity but the ground truth is anti_longevity. MBA1 is anti-longevity in yeast, meaning its deletion extends lifespan rather than shortening it. The model's reasoning assumes that because MBA1 supports mitochondrial translation and OXPHOS assembly, its loss would be harmful and thus the gene must be pro-longevity. However, this logic is flawed — reduced mitochondrial translation/OXPHOS activity is actually associated with lifespan extension in yeast (similar to how mitochondrial dysfunction can paradoxically extend lifespan through hormesis or reduced ROS production from a less active respiratory chain). The model's mechanistic reasoning about the gene's function is broadly correct (MBA1 tethers mitoribosomes to the inner membrane), but the inference about longevity direction is wrong. The model was moderately confident (0.62) in the wrong direction.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}