ral-1
C. elegans
small monomeric GTPase
What the model saw
Gene: ral-1 Organism: Caenorhabditis elegans Known functions: small monomeric GTPase. G protein activity. GTP binding. GTPase activity.
View unredacted entry
small monomeric GTPase. G protein activity. GTP binding. GTPase activity.
Solver output
RAL-1 is a small monomeric GTPase of the Ras superfamily (RalA/RalB ortholog in C. elegans). In the context of aging, RAL GTPases function downstream of Ras signaling and interact with components of the exocyst complex and autophagy regulation. In C. elegans, ral-1 has been shown to act in a pathway that promotes longevity, partly by modulating vesicle trafficking and nutrient-sensing outputs downstream of Ras/MAPK. Small GTPase cycling (GTP binding and hydrolysis via intrinsic GTPase activity) positions RAL-1 as a molecular switch that, when active, can promote autophagic flux and stress responses that extend lifespan. Its role in exocyst-mediated secretion also connects it to altered intercellular communication, but the primary mechanistic link in C. elegans aging studies is through nutrient-sensing and Ras-related signaling networks.
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 reasoning about RAL-1 promoting longevity through autophagy and nutrient sensing is incorrect. In C. elegans, ral-1 is actually anti-longevity, meaning its loss or reduction extends lifespan. The model constructed a plausible-sounding but ultimately incorrect mechanistic narrative, incorrectly framing RAL-1 as a positive regulator of lifespan. The confidence of 0.62 is moderate but still wrong. The mechanism described (pro-autophagic, pro-longevity Ras signaling) is the opposite of what is observed.
Raw API responses
solver
{
"reasoning": "RAL-1 is a small monomeric GTPase of the Ras superfamily (RalA/RalB ortholog in C. elegans). In the context of aging, RAL GTPases function downstream of Ras signaling and interact with components of the exocyst complex and autophagy regulation. In C. elegans, ral-1 has been shown to act in a pathway that promotes longevity, partly by modulating vesicle trafficking and nutrient-sensing outputs downstream of Ras/MAPK. Small GTPase cycling (GTP binding and hydrolysis via intrinsic GTPase activity) positions RAL-1 as a molecular switch that, when active, can promote autophagic flux and stress responses that extend lifespan. Its role in exocyst-mediated secretion also connects it to altered intercellular communication, but the primary mechanistic link in C. elegans aging studies is through nutrient-sensing and Ras-related signaling networks.",
"confidence": 0.62,
"key_pathways": [
"Ras/RalGEF/RAL GTPase signaling",
"exocyst complex and vesicle trafficking",
"autophagy regulation downstream of nutrient sensing"
],
"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 reasoning about RAL-1 promoting longevity through autophagy and nutrient sensing is incorrect. In C. elegans, ral-1 is actually anti-longevity, meaning its loss or reduction extends lifespan. The model constructed a plausible-sounding but ultimately incorrect mechanistic narrative, incorrectly framing RAL-1 as a positive regulator of lifespan. The confidence of 0.62 is moderate but still wrong. The mechanism described (pro-autophagic, pro-longevity Ras signaling) is the opposite of what is observed.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}