try-1
C. elegans
Peptidase S1 domain-containing protein
What the model saw
Gene: try-1 Organism: Caenorhabditis elegans Known functions: Peptidase S1 domain-containing protein. serine-type endopeptidase activity. serine-type peptidase activity.
View unredacted entry
Peptidase S1 domain-containing protein. serine-type endopeptidase activity. serine-type peptidase activity.
Solver output
try-1 encodes a trypsin-like serine endopeptidase (Peptidase S1 family) in C. elegans, functioning in proteolytic digestion of dietary proteins in the intestinal lumen. Efficient nutrient extraction via digestive proteases enhances amino acid availability, which feeds into nutrient-sensing pathways such as TOR/TORC1 signaling. Elevated TOR activity driven by increased amino acid flux is well-established as pro-aging in C. elegans, as it suppresses autophagy and stress responses. Conversely, reduced digestive protease activity (or dietary restriction) dampens TOR signaling and extends lifespan. Thus, the normal pro-digestive function of try-1 is expected to promote nutrient-sensing pathway activation, opposing longevity.
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 correctly predicted anti_longevity for try-1, but the mechanistic reasoning is speculative and likely incorrect. The model constructs an indirect chain: trypsin-like protease → better nutrient digestion → increased amino acid flux → TOR activation → pro-aging. This is a plausible-sounding but highly speculative mechanism with no direct evidence cited. The actual mechanism by which try-1 acts as anti-longevity in C. elegans is not well-established in the literature as a TOR/nutrient sensing pathway gene. The model essentially reverse-engineered a mechanism from first principles rather than citing known biology. The confidence of 0.62 is reasonable given the uncertainty, but the mechanistic class "deregulated_nutrient_sensing" is likely wrong - try-1 is more likely involved in direct proteolytic functions affecting aging through other means (e.g., protein quality control, immune function, or other pathways). The reasoning quality is low because it relies on an indirect, speculative chain of logic rather than established evidence.
Raw API responses
solver
{
"reasoning": "try-1 encodes a trypsin-like serine endopeptidase (Peptidase S1 family) in C. elegans, functioning in proteolytic digestion of dietary proteins in the intestinal lumen. Efficient nutrient extraction via digestive proteases enhances amino acid availability, which feeds into nutrient-sensing pathways such as TOR/TORC1 signaling. Elevated TOR activity driven by increased amino acid flux is well-established as pro-aging in C. elegans, as it suppresses autophagy and stress responses. Conversely, reduced digestive protease activity (or dietary restriction) dampens TOR signaling and extends lifespan. Thus, the normal pro-digestive function of try-1 is expected to promote nutrient-sensing pathway activation, opposing longevity.",
"confidence": 0.62,
"key_pathways": [
"TOR/TORC1 nutrient sensing",
"intestinal proteolysis and amino acid absorption",
"dietary restriction signaling"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for try-1, but the mechanistic reasoning is speculative and likely incorrect. The model constructs an indirect chain: trypsin-like protease → better nutrient digestion → increased amino acid flux → TOR activation → pro-aging. This is a plausible-sounding but highly speculative mechanism with no direct evidence cited. The actual mechanism by which try-1 acts as anti-longevity in C. elegans is not well-established in the literature as a TOR/nutrient sensing pathway gene. The model essentially reverse-engineered a mechanism from first principles rather than citing known biology. The confidence of 0.62 is reasonable given the uncertainty, but the mechanistic class \"deregulated_nutrient_sensing\" is likely wrong - try-1 is more likely involved in direct proteolytic functions affecting aging through other means (e.g., protein quality control, immune function, or other pathways). The reasoning quality is low because it relies on an indirect, speculative chain of logic rather than established evidence.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": true,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}