AKL1
S. cerevisiae
serine/threonine protein kinase AKL1
What the model saw
Gene: AKL1 Organism: Saccharomyces cerevisiae Known functions: serine/threonine protein kinase AKL1. ATP binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
View unredacted entry
serine/threonine protein kinase AKL1. ATP binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
Solver output
AKL1 (Ark1/Prk1-like kinase 1) is a serine/threonine protein kinase in S. cerevisiae with ATP-binding and protein phosphorylation activity. While serine/threonine kinases are central to nutrient-sensing pathways (e.g., TORC1, PKA, Snf1/AMPK) that strongly influence yeast longevity, AKL1 is primarily implicated in endocytic trafficking and actin patch regulation rather than canonical longevity-associated signaling cascades. Its molecular function annotations are too general to confidently assign a pro- or anti-longevity role, as serine/threonine kinases can either promote or oppose aging depending on their specific substrates and pathway context. Without evidence linking AKL1 directly to TOR, PKA, or Snf1 signaling, or to known longevity regulators, the prediction remains ambiguous.
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 "unclear" while the ground truth is "anti_longevity." The model correctly identified AKL1's role in endocytic trafficking and actin patch regulation, but failed to connect this to a longevity influence. The model's uncertainty was somewhat reasonable given the limited information provided, but it still got the answer wrong. The mechanism class of "deregulated_nutrient_sensing" is also incorrect - AKL1's anti-longevity role is more likely related to its endocytic/actin functions rather than nutrient sensing. The confidence of 0.35 reflects appropriate uncertainty, but the model should have leaned toward anti_longevity given that deletion of anti-longevity genes typically extends lifespan, and kinases involved in endocytic trafficking can negatively regulate longevity pathways.
Raw API responses
solver
{
"reasoning": "AKL1 (Ark1/Prk1-like kinase 1) is a serine/threonine protein kinase in S. cerevisiae with ATP-binding and protein phosphorylation activity. While serine/threonine kinases are central to nutrient-sensing pathways (e.g., TORC1, PKA, Snf1/AMPK) that strongly influence yeast longevity, AKL1 is primarily implicated in endocytic trafficking and actin patch regulation rather than canonical longevity-associated signaling cascades. Its molecular function annotations are too general to confidently assign a pro- or anti-longevity role, as serine/threonine kinases can either promote or oppose aging depending on their specific substrates and pathway context. Without evidence linking AKL1 directly to TOR, PKA, or Snf1 signaling, or to known longevity regulators, the prediction remains ambiguous.",
"confidence": 0.35,
"key_pathways": [
"serine/threonine phosphorylation signaling",
"endocytic trafficking / actin patch regulation",
"nutrient-sensing kinase networks"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity.\" The model correctly identified AKL1's role in endocytic trafficking and actin patch regulation, but failed to connect this to a longevity influence. The model's uncertainty was somewhat reasonable given the limited information provided, but it still got the answer wrong. The mechanism class of \"deregulated_nutrient_sensing\" is also incorrect - AKL1's anti-longevity role is more likely related to its endocytic/actin functions rather than nutrient sensing. The confidence of 0.35 reflects appropriate uncertainty, but the model should have leaned toward anti_longevity given that deletion of anti-longevity genes typically extends lifespan, and kinases involved in endocytic trafficking can negatively regulate longevity pathways.",
"failure_mode": "appropriately_uncertain",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}