cher
D. melanogaster
cheerio
What the model saw
Gene: cher Organism: Drosophila melanogaster Known functions: cheerio. actin binding. actin filament binding. protein binding.
View unredacted entry
cheerio. actin binding. actin filament binding. protein binding.
Solver output
The cheerio (cher) gene encodes a Drosophila filamin/actin-crosslinking protein with actin binding and actin filament binding activities. Filamins primarily function in cytoskeletal organization, cell shape maintenance, and mechanosensing by crosslinking actin filaments into networks. While actin cytoskeleton integrity is important for cellular function, the direct connection of filamin-mediated actin crosslinking to canonical longevity pathways (e.g., insulin/IGF-1 signaling, TOR, autophagy) is not well established. The protein binding annotation is too broad to resolve a specific pro- or anti-longevity mechanism, and filamin proteins can play roles in both tissue homeostasis (potentially pro-longevity) and signaling scaffolding that could go either way.
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 "pro_longevity." The model correctly identified cher as a filamin/actin-crosslinking protein and described its cytoskeletal functions, but failed to connect it to a pro-longevity role. The reasoning is plausible but overly hedged — the model acknowledged tissue homeostasis as a potential pro-longevity mechanism but ultimately declined to commit. The mechanistic reasoning is incomplete since it doesn't identify the specific pathway through which cher promotes longevity in Drosophila. Confidence was appropriately low (0.35), reflecting genuine uncertainty, but the answer is still wrong.
Raw API responses
solver
{
"reasoning": "The cheerio (cher) gene encodes a Drosophila filamin/actin-crosslinking protein with actin binding and actin filament binding activities. Filamins primarily function in cytoskeletal organization, cell shape maintenance, and mechanosensing by crosslinking actin filaments into networks. While actin cytoskeleton integrity is important for cellular function, the direct connection of filamin-mediated actin crosslinking to canonical longevity pathways (e.g., insulin/IGF-1 signaling, TOR, autophagy) is not well established. The protein binding annotation is too broad to resolve a specific pro- or anti-longevity mechanism, and filamin proteins can play roles in both tissue homeostasis (potentially pro-longevity) and signaling scaffolding that could go either way.",
"confidence": 0.35,
"key_pathways": [
"actin cytoskeleton organization",
"filamin-mediated actin crosslinking",
"mechanosensing and cell shape maintenance"
],
"mechanism_class": "other",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" while the ground truth is \"pro_longevity.\" The model correctly identified cher as a filamin/actin-crosslinking protein and described its cytoskeletal functions, but failed to connect it to a pro-longevity role. The reasoning is plausible but overly hedged — the model acknowledged tissue homeostasis as a potential pro-longevity mechanism but ultimately declined to commit. The mechanistic reasoning is incomplete since it doesn't identify the specific pathway through which cher promotes longevity in Drosophila. Confidence was appropriately low (0.35), reflecting genuine uncertainty, but the answer is still wrong.",
"failure_mode": "appropriately_uncertain",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}