EcR
D. melanogaster
Ecdysone receptor
What the model saw
Gene: EcR Organism: Drosophila melanogaster Known functions: Ecdysone receptor. ecdysone receptor. DNA binding. DNA-binding transcription activator activity, RNA polymerase II-specific. DNA-binding transcription factor activity. DNA-binding transcription factor activity, RNA polymerase II-specific. DNA-binding transcription factor binding. RNA polymerase II cis-regulatory region sequence-specific DNA binding. RNA polymerase II transcription regulatory region sequence-specific DNA binding. core promoter sequence-specific DNA binding. ecdysone binding. nuclear receptor activity. protein binding. protein heterodimerization activity. protein homodimerization activity. sequence-specific DNA binding. signaling receptor binding. small molecule binding. steroid binding. transcription cis-regulatory region binding. transcription coactivator binding. transcription corepressor binding. zinc ion binding.
View unredacted entry
Ecdysone receptor. ecdysone receptor. DNA binding. DNA-binding transcription activator activity, RNA polymerase II-specific. DNA-binding transcription factor activity. DNA-binding transcription factor activity, RNA polymerase II-specific. DNA-binding transcription factor binding. RNA polymerase II cis-regulatory region sequence-specific DNA binding. RNA polymerase II transcription regulatory region sequence-specific DNA binding. core promoter sequence-specific DNA binding. ecdysone binding. nuclear receptor activity. protein binding. protein heterodimerization activity. protein homodimerization activity. sequence-specific DNA binding. signaling receptor binding. small molecule binding. steroid binding. transcription cis-regulatory region binding. transcription coactivator binding. transcription corepressor binding. zinc ion binding.
Solver output
EcR encodes the Drosophila ecdysone receptor, a nuclear hormone receptor that heterodimerizes with Ultraspiracle (USP, the RXR ortholog) to mediate ecdysone signaling. Ecdysone signaling intersects with insulin/IGF-1 and nutrient-sensing pathways to coordinate developmental timing, metabolic homeostasis, and stress responses. In adult Drosophila, reduced or tissue-specific modulation of ecdysone signaling—particularly in the fat body and neurons—has been linked to extended lifespan, analogous to reduced IIS/TOR signaling. EcR acts as a ligand-activated transcription factor that, when properly regulated in adulthood, can promote expression of stress-resistance and metabolic genes. However, the relationship is context-dependent: ecdysone signaling promotes developmental transitions but its chronic activation in adults can be detrimental, while its role in coordinating reproductive-somatic trade-offs (via USP/RXR) places it within the deregulated nutrient-sensing hallmark. Overall, EcR's normal function in modulating steroid hormone-driven transcriptional programs is net pro-longevity when appropriately regulated in the adult stage.
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 acknowledges the context-dependence of ecdysone signaling but ultimately concludes incorrectly that EcR is net pro-longevity. In reality, EcR is anti-longevity in Drosophila — ecdysone signaling through EcR tends to shorten lifespan, and reducing EcR activity in adults extends lifespan. The model's reasoning is partially aware of this (noting "chronic activation in adults can be detrimental") but then contradicts itself by concluding pro-longevity. The mechanism class of "deregulated_nutrient_sensing" is also questionable — EcR is primarily a steroid hormone receptor, not a nutrient sensor per se. The confidence of 0.65 is moderately high for a wrong answer.
Raw API responses
solver
{
"reasoning": "EcR encodes the Drosophila ecdysone receptor, a nuclear hormone receptor that heterodimerizes with Ultraspiracle (USP, the RXR ortholog) to mediate ecdysone signaling. Ecdysone signaling intersects with insulin/IGF-1 and nutrient-sensing pathways to coordinate developmental timing, metabolic homeostasis, and stress responses. In adult Drosophila, reduced or tissue-specific modulation of ecdysone signaling—particularly in the fat body and neurons—has been linked to extended lifespan, analogous to reduced IIS/TOR signaling. EcR acts as a ligand-activated transcription factor that, when properly regulated in adulthood, can promote expression of stress-resistance and metabolic genes. However, the relationship is context-dependent: ecdysone signaling promotes developmental transitions but its chronic activation in adults can be detrimental, while its role in coordinating reproductive-somatic trade-offs (via USP/RXR) places it within the deregulated nutrient-sensing hallmark. Overall, EcR's normal function in modulating steroid hormone-driven transcriptional programs is net pro-longevity when appropriately regulated in the adult stage.",
"confidence": 0.65,
"key_pathways": [
"ecdysone/nuclear hormone receptor signaling",
"insulin/IGF-1 and nutrient-sensing pathway crosstalk",
"steroid hormone-regulated transcription via EcR-USP heterodimer"
],
"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 acknowledges the context-dependence of ecdysone signaling but ultimately concludes incorrectly that EcR is net pro-longevity. In reality, EcR is anti-longevity in Drosophila — ecdysone signaling through EcR tends to shorten lifespan, and reducing EcR activity in adults extends lifespan. The model's reasoning is partially aware of this (noting \"chronic activation in adults can be detrimental\") but then contradicts itself by concluding pro-longevity. The mechanism class of \"deregulated_nutrient_sensing\" is also questionable — EcR is primarily a steroid hormone receptor, not a nutrient sensor per se. The confidence of 0.65 is moderately high for a wrong answer.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}