INM1
S. cerevisiae
inositol monophosphate 1-phosphatase INM1
What the model saw
Gene: INM1 Organism: Saccharomyces cerevisiae Known functions: inositol monophosphate 1-phosphatase INM1. inositol monophosphate 1-phosphatase activity. inositol monophosphate phosphatase activity.
View unredacted entry
inositol monophosphate 1-phosphatase INM1. inositol monophosphate 1-phosphatase activity. inositol monophosphate phosphatase activity.
Solver output
INM1 encodes an inositol monophosphate 1-phosphatase that catalyzes the dephosphorylation of inositol monophosphate (IMP) to free inositol, a key step in the inositol biosynthesis pathway. Inositol is a critical precursor for phosphoinositides (PI, PI3P, PI4P, PIP2, etc.), which are central signaling lipids regulating TOR pathway activity, autophagy initiation, and membrane trafficking. Adequate inositol availability supports proper phosphoinositide signaling, which in yeast is linked to nutrient sensing and stress responses. Inositol depletion or dysregulation of inositol metabolism has been associated with altered TOR signaling and reduced cellular fitness. By maintaining inositol homeostasis, INM1 supports balanced phosphoinositide-dependent signaling, potentially moderating pro-aging nutrient-sensing pathways. However, the direct evidence linking INM1 specifically to lifespan extension in yeast is limited, moderating confidence in this prediction.
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 predicted pro_longevity while the ground truth is anti_longevity. INM1 is an anti-longevity gene, meaning its deletion extends lifespan. The model's reasoning focused on INM1 maintaining inositol homeostasis and supporting balanced signaling, leading it to conclude the gene is pro-longevity. However, the actual finding is that INM1 activity shortens lifespan (i.e., it is anti-longevity). The mechanistic reasoning about inositol biosynthesis and phosphoinositide signaling is plausible but leads to the wrong conclusion. The model acknowledged limited direct evidence but still predicted the wrong direction. Confidence was moderate (0.55), so not extremely overconfident, but still wrong.
Raw API responses
solver
{
"reasoning": "INM1 encodes an inositol monophosphate 1-phosphatase that catalyzes the dephosphorylation of inositol monophosphate (IMP) to free inositol, a key step in the inositol biosynthesis pathway. Inositol is a critical precursor for phosphoinositides (PI, PI3P, PI4P, PIP2, etc.), which are central signaling lipids regulating TOR pathway activity, autophagy initiation, and membrane trafficking. Adequate inositol availability supports proper phosphoinositide signaling, which in yeast is linked to nutrient sensing and stress responses. Inositol depletion or dysregulation of inositol metabolism has been associated with altered TOR signaling and reduced cellular fitness. By maintaining inositol homeostasis, INM1 supports balanced phosphoinositide-dependent signaling, potentially moderating pro-aging nutrient-sensing pathways. However, the direct evidence linking INM1 specifically to lifespan extension in yeast is limited, moderating confidence in this prediction.",
"confidence": 0.55,
"key_pathways": [
"inositol biosynthesis and phosphoinositide signaling",
"TOR nutrient sensing pathway",
"autophagy regulation via PI3P"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity while the ground truth is anti_longevity. INM1 is an anti-longevity gene, meaning its deletion extends lifespan. The model's reasoning focused on INM1 maintaining inositol homeostasis and supporting balanced signaling, leading it to conclude the gene is pro-longevity. However, the actual finding is that INM1 activity shortens lifespan (i.e., it is anti-longevity). The mechanistic reasoning about inositol biosynthesis and phosphoinositide signaling is plausible but leads to the wrong conclusion. The model acknowledged limited direct evidence but still predicted the wrong direction. Confidence was moderate (0.55), so not extremely overconfident, but still wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}