SDP1
S. cerevisiae
mitogen-activated protein kinase tyrosine protein phosphatase SDP1
What the model saw
Gene: SDP1 Organism: Saccharomyces cerevisiae Known functions: mitogen-activated protein kinase tyrosine protein phosphatase SDP1. MAP kinase tyrosine phosphatase activity. MAP kinase tyrosine/serine/threonine phosphatase activity. protein tyrosine phosphatase activity. protein tyrosine/serine/threonine phosphatase activity. protein tyrosine/threonine phosphatase activity.
View unredacted entry
mitogen-activated protein kinase tyrosine protein phosphatase SDP1. MAP kinase tyrosine phosphatase activity. MAP kinase tyrosine/serine/threonine phosphatase activity. protein tyrosine phosphatase activity. protein tyrosine/serine/threonine phosphatase activity. protein tyrosine/threonine phosphatase activity.
Solver output
SDP1 is a dual-specificity MAP kinase phosphatase (MKP) in S. cerevisiae that dephosphorylates and inactivates MAP kinases on both tyrosine and threonine/serine residues. By negatively regulating MAPK signaling—particularly stress-responsive pathways such as the HOG (Hog1) and cell integrity (Slt2/Mpk1) pathways—SDP1 dampens adaptive stress responses that are critical for longevity. Hog1, a key target of MKPs, is a functional ortholog of p38 MAPK and promotes stress resistance, osmoadaptation, and longevity when active; its inactivation by SDP1 would therefore be anti-longevity. Additionally, MAPK cascades in yeast intersect with nutrient-sensing networks (TOR, Ras/PKA), and attenuation of these stress-responsive kinases by SDP1 reduces the cell's capacity to mount protective responses. Thus, the normal phosphatase function of SDP1 opposes longevity by curtailing pro-survival MAPK activity.
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 SDP1. The mechanistic reasoning is sound: SDP1 is a dual-specificity MAP kinase phosphatase that inactivates stress-responsive MAPK pathways (HOG/Hog1), and dampening these pro-survival pathways would be anti-longevity. The reasoning is well-grounded in yeast biology. The mechanism class "deregulated_nutrient_sensing" is a slight stretch since the primary mechanism is more directly about stress-response MAPK inactivation rather than nutrient sensing per se, but the model does acknowledge the MAPK-TOR crosstalk. Overall, the prediction and reasoning are solid.
Raw API responses
solver
{
"reasoning": "SDP1 is a dual-specificity MAP kinase phosphatase (MKP) in S. cerevisiae that dephosphorylates and inactivates MAP kinases on both tyrosine and threonine/serine residues. By negatively regulating MAPK signaling—particularly stress-responsive pathways such as the HOG (Hog1) and cell integrity (Slt2/Mpk1) pathways—SDP1 dampens adaptive stress responses that are critical for longevity. Hog1, a key target of MKPs, is a functional ortholog of p38 MAPK and promotes stress resistance, osmoadaptation, and longevity when active; its inactivation by SDP1 would therefore be anti-longevity. Additionally, MAPK cascades in yeast intersect with nutrient-sensing networks (TOR, Ras/PKA), and attenuation of these stress-responsive kinases by SDP1 reduces the cell's capacity to mount protective responses. Thus, the normal phosphatase function of SDP1 opposes longevity by curtailing pro-survival MAPK activity.",
"confidence": 0.72,
"key_pathways": [
"HOG (Hog1 MAPK) stress response pathway",
"Cell wall integrity (Slt2/Mpk1 MAPK) pathway",
"MAPK-TOR nutrient sensing crosstalk"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for SDP1. The mechanistic reasoning is sound: SDP1 is a dual-specificity MAP kinase phosphatase that inactivates stress-responsive MAPK pathways (HOG/Hog1), and dampening these pro-survival pathways would be anti-longevity. The reasoning is well-grounded in yeast biology. The mechanism class \"deregulated_nutrient_sensing\" is a slight stretch since the primary mechanism is more directly about stress-response MAPK inactivation rather than nutrient sensing per se, but the model does acknowledge the MAPK-TOR crosstalk. Overall, the prediction and reasoning are solid.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}