adr-1
C. elegans
A-to-I RNA editing regulator adr-1
What the model saw
Gene: adr-1 Organism: Caenorhabditis elegans Known functions: A-to-I RNA editing regulator adr-1. RNA binding. adenosine deaminase activity. double-stranded RNA adenosine deaminase activity. mRNA binding.
View unredacted entry
A-to-I RNA editing regulator adr-1. RNA binding. adenosine deaminase activity. double-stranded RNA adenosine deaminase activity. mRNA binding.
Solver output
ADR-1 is an adenosine deaminase acting on RNA (ADAR), catalyzing A-to-I editing of double-stranded RNA substrates. A-to-I RNA editing is a post-transcriptional epitranscriptomic mechanism that diversifies the transcriptome and modulates innate immune sensing by preventing endogenous dsRNA from triggering aberrant interferon/antiviral responses. In C. elegans, loss of ADAR activity leads to accumulation of unedited dsRNA, which can activate innate immune pathways and promote chronic inflammation-like signaling — a hallmark associated with accelerated aging. Additionally, A-to-I editing can recode specific mRNAs (e.g., ion channels, signaling molecules), fine-tuning neuronal and cellular function relevant to organismal healthspan. By maintaining proper epitranscriptomic regulation and suppressing aberrant dsRNA-triggered immune activation, adr-1 is predicted to support longevity.
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 adr-1. The mechanistic reasoning is plausible and biologically coherent — ADAR/A-to-I editing suppressing aberrant dsRNA-triggered immune activation is a reasonable mechanism for longevity support. However, the reasoning is somewhat speculative and extrapolated from mammalian biology (interferon responses don't directly apply to C. elegans in the same way), and the model's confidence is appropriately modest at 0.55. The classification as "epigenetic_alterations" is debatable since A-to-I RNA editing is more accurately an epitranscriptomic/post-transcriptional mechanism rather than a classic epigenetic alteration, but the model does acknowledge this distinction in its reasoning. Overall, the prediction is correct with reasonable mechanistic support.
Raw API responses
solver
{
"reasoning": "ADR-1 is an adenosine deaminase acting on RNA (ADAR), catalyzing A-to-I editing of double-stranded RNA substrates. A-to-I RNA editing is a post-transcriptional epitranscriptomic mechanism that diversifies the transcriptome and modulates innate immune sensing by preventing endogenous dsRNA from triggering aberrant interferon/antiviral responses. In C. elegans, loss of ADAR activity leads to accumulation of unedited dsRNA, which can activate innate immune pathways and promote chronic inflammation-like signaling — a hallmark associated with accelerated aging. Additionally, A-to-I editing can recode specific mRNAs (e.g., ion channels, signaling molecules), fine-tuning neuronal and cellular function relevant to organismal healthspan. By maintaining proper epitranscriptomic regulation and suppressing aberrant dsRNA-triggered immune activation, adr-1 is predicted to support longevity.",
"confidence": 0.55,
"key_pathways": [
"A-to-I RNA editing (epitranscriptomics)",
"innate immune dsRNA sensing suppression",
"mRNA recoding and post-transcriptional regulation"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for adr-1. The mechanistic reasoning is plausible and biologically coherent — ADAR/A-to-I editing suppressing aberrant dsRNA-triggered immune activation is a reasonable mechanism for longevity support. However, the reasoning is somewhat speculative and extrapolated from mammalian biology (interferon responses don't directly apply to C. elegans in the same way), and the model's confidence is appropriately modest at 0.55. The classification as \"epigenetic_alterations\" is debatable since A-to-I RNA editing is more accurately an epitranscriptomic/post-transcriptional mechanism rather than a classic epigenetic alteration, but the model does acknowledge this distinction in its reasoning. Overall, the prediction is correct with reasonable mechanistic support.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}