scd-2
C. elegans
ALK tyrosine kinase receptor homolog scd-2
What the model saw
Gene: scd-2 Organism: Caenorhabditis elegans Known functions: ALK tyrosine kinase receptor homolog scd-2. ATP binding. protein kinase activity. protein tyrosine kinase activity. transmembrane receptor protein tyrosine kinase activity.
View unredacted entry
ALK tyrosine kinase receptor homolog scd-2. ATP binding. protein kinase activity. protein tyrosine kinase activity. transmembrane receptor protein tyrosine kinase activity.
Solver output
SCD-2 is the C. elegans homolog of the ALK (Anaplastic Lymphoma Kinase) receptor tyrosine kinase. As a transmembrane receptor protein tyrosine kinase with ATP binding and kinase activity, SCD-2 transduces extracellular signals into intracellular growth and proliferation pathways. ALK receptor tyrosine kinases canonically activate downstream pro-growth signaling cascades including RAS/MAPK and PI3K/AKT pathways. In C. elegans, activation of insulin/IGF-1-like receptor tyrosine kinase signaling (via DAF-2) is well established to shorten lifespan by suppressing the FOXO transcription factor DAF-16. SCD-2/ALK similarly promotes anabolic, growth-promoting signaling that antagonizes stress resistance and longevity pathways. Loss-of-function of scd-2 has been associated with extended lifespan in C. elegans, consistent with the general principle that attenuation of receptor tyrosine kinase/nutrient-sensing signaling promotes 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 predicted anti_longevity for scd-2, but the ground truth is pro_longevity. The model's reasoning follows a plausible but incorrect analogy to DAF-2/insulin signaling, assuming that receptor tyrosine kinases generally shorten lifespan. In reality, scd-2 (ALK homolog in C. elegans) is pro-longevity — loss of scd-2 shortens lifespan rather than extending it. The model even explicitly states "Loss-of-function of scd-2 has been associated with extended lifespan," which is the opposite of what the ground truth indicates. The model was fairly confident (0.72) in its wrong answer. The mechanistic reasoning about ALK activating RAS/MAPK and PI3K/AKT pathways is partially plausible in general terms, but the conclusion drawn (anti_longevity) is incorrect for this specific gene in C. elegans.
Raw API responses
solver
{
"reasoning": "SCD-2 is the C. elegans homolog of the ALK (Anaplastic Lymphoma Kinase) receptor tyrosine kinase. As a transmembrane receptor protein tyrosine kinase with ATP binding and kinase activity, SCD-2 transduces extracellular signals into intracellular growth and proliferation pathways. ALK receptor tyrosine kinases canonically activate downstream pro-growth signaling cascades including RAS/MAPK and PI3K/AKT pathways. In C. elegans, activation of insulin/IGF-1-like receptor tyrosine kinase signaling (via DAF-2) is well established to shorten lifespan by suppressing the FOXO transcription factor DAF-16. SCD-2/ALK similarly promotes anabolic, growth-promoting signaling that antagonizes stress resistance and longevity pathways. Loss-of-function of scd-2 has been associated with extended lifespan in C. elegans, consistent with the general principle that attenuation of receptor tyrosine kinase/nutrient-sensing signaling promotes longevity.",
"confidence": 0.72,
"key_pathways": [
"ALK/RAS/MAPK signaling",
"PI3K/AKT/DAF-16 (FOXO) axis",
"insulin/IGF-1-like receptor tyrosine kinase signaling"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model predicted anti_longevity for scd-2, but the ground truth is pro_longevity. The model's reasoning follows a plausible but incorrect analogy to DAF-2/insulin signaling, assuming that receptor tyrosine kinases generally shorten lifespan. In reality, scd-2 (ALK homolog in C. elegans) is pro-longevity — loss of scd-2 shortens lifespan rather than extending it. The model even explicitly states \"Loss-of-function of scd-2 has been associated with extended lifespan,\" which is the opposite of what the ground truth indicates. The model was fairly confident (0.72) in its wrong answer. The mechanistic reasoning about ALK activating RAS/MAPK and PI3K/AKT pathways is partially plausible in general terms, but the conclusion drawn (anti_longevity) is incorrect for this specific gene in C. elegans.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}