elav
D. melanogaster
embryonic lethal abnormal vision
What the model saw
Gene: elav Organism: Drosophila melanogaster Known functions: embryonic lethal abnormal vision. RNA binding. mRNA binding. mRNA regulatory element binding translation repressor activity. nucleic acid binding. poly(U) RNA binding. protein-RNA adaptor activity.
View unredacted entry
embryonic lethal abnormal vision. RNA binding. mRNA binding. mRNA regulatory element binding translation repressor activity. nucleic acid binding. poly(U) RNA binding. protein-RNA adaptor activity.
Solver output
ELAV (Embryonic Lethal Abnormal Vision) is a founding member of the HuR/ELAVL family of RNA-binding proteins that bind AU-rich elements and poly(U) sequences in mRNA 3' UTRs, stabilizing target transcripts and regulating their translation. In Drosophila, elav is essential for neuronal differentiation and maintenance, acting as a translational repressor and mRNA stabilizer for key neuronal transcripts. Loss of elav function leads to neurodegeneration and premature neuronal death, consistent with an anti-aging role in the nervous system. Its protein-RNA adaptor activity positions it as a post-transcriptional regulator of proteostasis and stress-response mRNAs in neurons, pathways critically linked to organismal longevity. Maintenance of neuronal integrity through RNA stabilization is a well-established pro-longevity mechanism in Drosophila, and ELAV orthologs (e.g., HuD/ELAVL4) are similarly neuroprotective in mammals.
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 correctly predicted pro_longevity for elav in Drosophila melanogaster. The mechanistic reasoning is sound and well-grounded: ELAV is an RNA-binding protein critical for neuronal maintenance, and loss of function leads to neurodegeneration, consistent with a pro-longevity role. The model appropriately connects neuronal integrity via mRNA stabilization to longevity. The reasoning about HuR/ELAVL family, AU-rich element binding, and neuroprotection is accurate. Confidence of 0.72 is reasonable. Minor note: the model could have been more specific about direct experimental evidence in Drosophila longevity studies, but the overall mechanistic framework is correct.
Raw API responses
solver
{
"reasoning": "ELAV (Embryonic Lethal Abnormal Vision) is a founding member of the HuR/ELAVL family of RNA-binding proteins that bind AU-rich elements and poly(U) sequences in mRNA 3' UTRs, stabilizing target transcripts and regulating their translation. In Drosophila, elav is essential for neuronal differentiation and maintenance, acting as a translational repressor and mRNA stabilizer for key neuronal transcripts. Loss of elav function leads to neurodegeneration and premature neuronal death, consistent with an anti-aging role in the nervous system. Its protein-RNA adaptor activity positions it as a post-transcriptional regulator of proteostasis and stress-response mRNAs in neurons, pathways critically linked to organismal longevity. Maintenance of neuronal integrity through RNA stabilization is a well-established pro-longevity mechanism in Drosophila, and ELAV orthologs (e.g., HuD/ELAVL4) are similarly neuroprotective in mammals.",
"confidence": 0.72,
"key_pathways": [
"neuronal mRNA stabilization and post-transcriptional regulation",
"translational repression of AU-rich element-containing transcripts",
"neuronal maintenance and neuroprotection"
],
"mechanism_class": "other",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for elav in Drosophila melanogaster. The mechanistic reasoning is sound and well-grounded: ELAV is an RNA-binding protein critical for neuronal maintenance, and loss of function leads to neurodegeneration, consistent with a pro-longevity role. The model appropriately connects neuronal integrity via mRNA stabilization to longevity. The reasoning about HuR/ELAVL family, AU-rich element binding, and neuroprotection is accurate. Confidence of 0.72 is reasonable. Minor note: the model could have been more specific about direct experimental evidence in Drosophila longevity studies, but the overall mechanistic framework is correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}