SDS23
S. cerevisiae
Sds23p
What the model saw
Gene: SDS23 Organism: Saccharomyces cerevisiae Known functions: Sds23p. protein serine/threonine phosphatase inhibitor activity.
View unredacted entry
Sds23p. protein serine/threonine phosphatase inhibitor activity.
Solver output
Sds23p functions as an inhibitor of protein serine/threonine phosphatases, most notably PP2A-type phosphatases (Pph21/Pph22) and the related phosphatase Ppg1. In yeast, PP2A and related phosphatases are key positive regulators of TORC1 signaling output and nutrient-sensing pathways; inhibiting these phosphatases can dampen anabolic signaling analogous to reducing TOR activity. By restraining PP2A-family phosphatase activity, Sds23p may promote a state of reduced nutrient-sensing signaling, which is broadly associated with lifespan extension in yeast. Additionally, Sds23p has been linked to cell cycle arrest under nutrient-limiting conditions, consistent with a role in coordinating growth restraint with environmental cues—a hallmark of pro-longevity interventions.
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 pro_longevity but the ground truth is anti_longevity. The model's mechanistic reasoning about PP2A inhibition reducing TOR-like signaling and thereby extending lifespan is plausible-sounding but ultimately incorrect in its conclusion. SDS23 is anti-longevity in yeast, meaning its deletion (loss of function) extends lifespan, not its presence. The model's logic that inhibiting PP2A-family phosphatases mimics reduced TOR activity is speculative and not well-supported; in reality, PP2A phosphatases have complex roles and inhibiting them does not straightforwardly reduce nutrient sensing in a pro-longevity manner. The model had moderate confidence (0.62) but still got both the answer and the mechanistic direction wrong.
Raw API responses
solver
{
"reasoning": "Sds23p functions as an inhibitor of protein serine/threonine phosphatases, most notably PP2A-type phosphatases (Pph21/Pph22) and the related phosphatase Ppg1. In yeast, PP2A and related phosphatases are key positive regulators of TORC1 signaling output and nutrient-sensing pathways; inhibiting these phosphatases can dampen anabolic signaling analogous to reducing TOR activity. By restraining PP2A-family phosphatase activity, Sds23p may promote a state of reduced nutrient-sensing signaling, which is broadly associated with lifespan extension in yeast. Additionally, Sds23p has been linked to cell cycle arrest under nutrient-limiting conditions, consistent with a role in coordinating growth restraint with environmental cues—a hallmark of pro-longevity interventions.",
"confidence": 0.62,
"key_pathways": [
"PP2A phosphatase inhibition",
"TORC1/nutrient-sensing signaling",
"cell cycle regulation under nutrient limitation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's mechanistic reasoning about PP2A inhibition reducing TOR-like signaling and thereby extending lifespan is plausible-sounding but ultimately incorrect in its conclusion. SDS23 is anti-longevity in yeast, meaning its deletion (loss of function) extends lifespan, not its presence. The model's logic that inhibiting PP2A-family phosphatases mimics reduced TOR activity is speculative and not well-supported; in reality, PP2A phosphatases have complex roles and inhibiting them does not straightforwardly reduce nutrient sensing in a pro-longevity manner. The model had moderate confidence (0.62) but still got both the answer and the mechanistic direction wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}