rsks-1
C. elegans
Ribosomal protein S6 kinase beta
What the model saw
Gene: rsks-1 Organism: Caenorhabditis elegans Known functions: Ribosomal protein S6 kinase beta. ATP binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
View unredacted entry
Ribosomal protein S6 kinase beta. ATP binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
Solver output
rsks-1 encodes the C. elegans ortholog of ribosomal protein S6 kinase beta (S6K1), a key downstream effector of the TOR (Target of Rapamycin) nutrient-sensing pathway. In the TOR signaling axis, activated TORC1 phosphorylates and activates S6K, which in turn phosphorylates ribosomal protein S6 and other substrates to promote mRNA translation and anabolic growth. Hyperactivation of this pathway suppresses autophagy and accelerates aging, while loss-of-function of rsks-1 is well-established to extend lifespan in C. elegans, phenocopying TOR inhibition. S6K also phosphorylates and inhibits IRS-1 (insulin receptor substrate), creating a negative feedback loop that dampens insulin/IGF-1 signaling, but the net effect of rsks-1 activity is pro-growth and anti-longevity. Genetic studies in worms confirm that rsks-1 null mutants live significantly longer, placing it firmly as an anti-longevity gene within the TOR/nutrient-sensing hallmark.
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 identified rsks-1 as anti_longevity with high confidence (0.93). The mechanistic reasoning is excellent and accurate: rsks-1 encodes the C. elegans S6K1 ortholog, a downstream effector of TORC1 nutrient-sensing. Loss-of-function of rsks-1 extends lifespan in C. elegans, confirming its anti-longevity role. The model correctly identifies the TOR pathway, translational control, and the IRS-1 negative feedback loop. All key pathways cited are relevant and accurate.
Raw API responses
solver
{
"reasoning": "rsks-1 encodes the C. elegans ortholog of ribosomal protein S6 kinase beta (S6K1), a key downstream effector of the TOR (Target of Rapamycin) nutrient-sensing pathway. In the TOR signaling axis, activated TORC1 phosphorylates and activates S6K, which in turn phosphorylates ribosomal protein S6 and other substrates to promote mRNA translation and anabolic growth. Hyperactivation of this pathway suppresses autophagy and accelerates aging, while loss-of-function of rsks-1 is well-established to extend lifespan in C. elegans, phenocopying TOR inhibition. S6K also phosphorylates and inhibits IRS-1 (insulin receptor substrate), creating a negative feedback loop that dampens insulin/IGF-1 signaling, but the net effect of rsks-1 activity is pro-growth and anti-longevity. Genetic studies in worms confirm that rsks-1 null mutants live significantly longer, placing it firmly as an anti-longevity gene within the TOR/nutrient-sensing hallmark.",
"confidence": 0.93,
"key_pathways": [
"TOR (TORC1) nutrient-sensing signaling",
"Ribosomal S6 kinase / translational control",
"Insulin/IGF-1 signaling (IRS-1 negative feedback)"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified rsks-1 as anti_longevity with high confidence (0.93). The mechanistic reasoning is excellent and accurate: rsks-1 encodes the C. elegans S6K1 ortholog, a downstream effector of TORC1 nutrient-sensing. Loss-of-function of rsks-1 extends lifespan in C. elegans, confirming its anti-longevity role. The model correctly identifies the TOR pathway, translational control, and the IRS-1 negative feedback loop. All key pathways cited are relevant and accurate.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}