ins-7
C. elegans
Insulin-like peptide 7;putative insulin-like peptide beta-type 4
What the model saw
Gene: ins-7 Organism: Caenorhabditis elegans Known functions: Insulin-like peptide 7;putative insulin-like peptide beta-type 4. hormone activity.
View unredacted entry
Insulin-like peptide 7;putative insulin-like peptide beta-type 4. hormone activity.
Solver output
INS-7 is an insulin-like peptide in C. elegans that acts as a ligand for the DAF-2 insulin/IGF-1 receptor. Activation of DAF-2 by insulin-like peptides triggers the PI3K/AKT signaling cascade, which phosphorylates and cytoplasmatically sequesters the FOXO transcription factor DAF-16. Nuclear DAF-16 is the primary driver of longevity gene expression in C. elegans, and its inhibition by insulin/IGF-1 signaling shortens lifespan. INS-7 has been specifically identified as an agonist of DAF-2, meaning its normal function suppresses DAF-16 nuclear activity and thus opposes longevity. Reduced insulin/IGF-1 signaling (e.g., daf-2 loss-of-function) dramatically extends lifespan in C. elegans, placing INS-7 as a pro-aging factor within this pathway.
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 ins-7. The mechanistic reasoning is accurate and detailed: INS-7 is indeed a DAF-2 agonist insulin-like peptide that activates the IIS pathway, suppresses DAF-16 nuclear activity, and thereby opposes longevity. The model correctly identifies the PI3K/AKT/DAF-16 axis and explains why INS-7 is a pro-aging factor. Confidence of 0.82 is appropriate given the well-established biology.
Raw API responses
solver
{
"reasoning": "INS-7 is an insulin-like peptide in C. elegans that acts as a ligand for the DAF-2 insulin/IGF-1 receptor. Activation of DAF-2 by insulin-like peptides triggers the PI3K/AKT signaling cascade, which phosphorylates and cytoplasmatically sequesters the FOXO transcription factor DAF-16. Nuclear DAF-16 is the primary driver of longevity gene expression in C. elegans, and its inhibition by insulin/IGF-1 signaling shortens lifespan. INS-7 has been specifically identified as an agonist of DAF-2, meaning its normal function suppresses DAF-16 nuclear activity and thus opposes longevity. Reduced insulin/IGF-1 signaling (e.g., daf-2 loss-of-function) dramatically extends lifespan in C. elegans, placing INS-7 as a pro-aging factor within this pathway.",
"confidence": 0.82,
"key_pathways": [
"insulin/IGF-1 signaling (IIS) pathway",
"DAF-2/DAF-16 axis",
"PI3K/AKT signaling"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for ins-7. The mechanistic reasoning is accurate and detailed: INS-7 is indeed a DAF-2 agonist insulin-like peptide that activates the IIS pathway, suppresses DAF-16 nuclear activity, and thereby opposes longevity. The model correctly identifies the PI3K/AKT/DAF-16 axis and explains why INS-7 is a pro-aging factor. Confidence of 0.82 is appropriate given the well-established biology.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}