amt-2
C. elegans
Putative ammonium transporter 2
What the model saw
Gene: amt-2 Organism: Caenorhabditis elegans Known functions: Putative ammonium transporter 2. ammonium channel activity.
View unredacted entry
Putative ammonium transporter 2. ammonium channel activity.
Solver output
amt-2 encodes a putative ammonium transporter with ammonium channel activity, facilitating the movement of NH4+/NH3 across membranes. Ammonium is a metabolic waste product of amino acid catabolism and nucleotide metabolism, and its accumulation can be toxic; however, ammonium transport also intersects with nitrogen sensing and amino acid metabolism pathways. While ammonium toxicity and nitrogen waste management could theoretically link to nutrient sensing or proteostasis, there is no well-established direct mechanistic connection between ammonium channel activity and canonical longevity pathways (e.g., IIS, TOR, DAF-16) in C. elegans. The molecular function annotation is too narrow and insufficiently characterized in the aging context to confidently assign a pro- or anti-longevity role.
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" with low confidence (0.35), while the ground truth is "anti_longevity." The model's reasoning is plausible but ultimately fails to commit to the correct answer. The model correctly identifies ammonium transport and nitrogen metabolism as relevant pathways, and even notes that ammonium accumulation can be toxic, which could hint at an anti-longevity role. However, it stops short of making a directional prediction. The reasoning quality is modest — it correctly identifies the gene's function but doesn't leverage the toxicity angle to make a directional call. This is a case of appropriate uncertainty given limited information, but the model still gets the answer wrong.
Raw API responses
solver
{
"reasoning": "amt-2 encodes a putative ammonium transporter with ammonium channel activity, facilitating the movement of NH4+/NH3 across membranes. Ammonium is a metabolic waste product of amino acid catabolism and nucleotide metabolism, and its accumulation can be toxic; however, ammonium transport also intersects with nitrogen sensing and amino acid metabolism pathways. While ammonium toxicity and nitrogen waste management could theoretically link to nutrient sensing or proteostasis, there is no well-established direct mechanistic connection between ammonium channel activity and canonical longevity pathways (e.g., IIS, TOR, DAF-16) in C. elegans. The molecular function annotation is too narrow and insufficiently characterized in the aging context to confidently assign a pro- or anti-longevity role.",
"confidence": 0.35,
"key_pathways": [
"ammonium/nitrogen transport",
"amino acid catabolism waste clearance",
"nitrogen metabolite homeostasis"
],
"mechanism_class": "unclear",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" with low confidence (0.35), while the ground truth is \"anti_longevity.\" The model's reasoning is plausible but ultimately fails to commit to the correct answer. The model correctly identifies ammonium transport and nitrogen metabolism as relevant pathways, and even notes that ammonium accumulation can be toxic, which could hint at an anti-longevity role. However, it stops short of making a directional prediction. The reasoning quality is modest — it correctly identifies the gene's function but doesn't leverage the toxicity angle to make a directional call. This is a case of appropriate uncertainty given limited information, but the model still gets the answer wrong.",
"failure_mode": "appropriately_uncertain",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}