MNN1
S. cerevisiae
alpha-1,3-mannosyltransferase MNN1
What the model saw
Gene: MNN1 Organism: Saccharomyces cerevisiae Known functions: alpha-1,3-mannosyltransferase MNN1. alpha-1,3-mannosyltransferase activity. glycosyltransferase activity. mannosyltransferase activity.
View unredacted entry
alpha-1,3-mannosyltransferase MNN1. alpha-1,3-mannosyltransferase activity. glycosyltransferase activity. mannosyltransferase activity.
Solver output
MNN1 encodes an alpha-1,3-mannosyltransferase responsible for adding terminal alpha-1,3-mannose residues to N-linked and O-linked glycans on cell wall and secreted proteins in S. cerevisiae. This function is primarily involved in protein glycosylation and cell wall integrity rather than any of the canonical aging hallmark pathways. While proper protein glycosylation can influence proteostasis indirectly, MNN1's specific role in terminal mannosylation of the outer chain does not have a well-established direct connection to lifespan regulation. Some evidence suggests that cell wall composition and glycosylation can affect stress responses, but the directionality of MNN1's influence on longevity is not clearly established in the literature. The molecular function annotations do not point to a clear pro- or anti-longevity mechanism through nutrient sensing, mitochondrial function, or other major aging pathways.
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 "unclear" while the ground truth is "anti_longevity." The model correctly described MNN1's biochemical function (alpha-1,3-mannosyltransferase involved in N-linked glycosylation and cell wall integrity) but failed to connect this to its known anti-longevity role. The model's reasoning that MNN1 lacks a "well-established direct connection to lifespan regulation" is incorrect per GenAge. The model was appropriately uncertain in tone but still gave the wrong categorical answer. The mechanism discussion is generic and doesn't capture why MNN1 deletion would extend lifespan (likely through effects on cell wall stress signaling or related pathways). Confidence was low (0.35), which is appropriate given the uncertainty, but the prediction was still wrong.
Raw API responses
solver
{
"reasoning": "MNN1 encodes an alpha-1,3-mannosyltransferase responsible for adding terminal alpha-1,3-mannose residues to N-linked and O-linked glycans on cell wall and secreted proteins in S. cerevisiae. This function is primarily involved in protein glycosylation and cell wall integrity rather than any of the canonical aging hallmark pathways. While proper protein glycosylation can influence proteostasis indirectly, MNN1's specific role in terminal mannosylation of the outer chain does not have a well-established direct connection to lifespan regulation. Some evidence suggests that cell wall composition and glycosylation can affect stress responses, but the directionality of MNN1's influence on longevity is not clearly established in the literature. The molecular function annotations do not point to a clear pro- or anti-longevity mechanism through nutrient sensing, mitochondrial function, or other major aging pathways.",
"confidence": 0.35,
"key_pathways": [
"N-linked glycosylation / mannan outer chain biosynthesis",
"cell wall integrity signaling",
"protein glycosylation and secretory pathway"
],
"mechanism_class": "other",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity.\" The model correctly described MNN1's biochemical function (alpha-1,3-mannosyltransferase involved in N-linked glycosylation and cell wall integrity) but failed to connect this to its known anti-longevity role. The model's reasoning that MNN1 lacks a \"well-established direct connection to lifespan regulation\" is incorrect per GenAge. The model was appropriately uncertain in tone but still gave the wrong categorical answer. The mechanism discussion is generic and doesn't capture why MNN1 deletion would extend lifespan (likely through effects on cell wall stress signaling or related pathways). Confidence was low (0.35), which is appropriate given the uncertainty, but the prediction was still wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}