cid-1
C. elegans
4Fe-4S ferredoxin-type domain-containing protein
What the model saw
Gene: cid-1 Organism: Caenorhabditis elegans Known functions: 4Fe-4S ferredoxin-type domain-containing protein. RNA uridylyltransferase activity. nucleic acid binding. poly(A) RNA polymerase activity. zinc ion binding.
View unredacted entry
4Fe-4S ferredoxin-type domain-containing protein. RNA uridylyltransferase activity. nucleic acid binding. poly(A) RNA polymerase activity. zinc ion binding.
Solver output
CID-1 (cytoplasmic poly(U) polymerase) is a terminal RNA uridylyltransferase (TUTase) in C. elegans that adds uridine residues to the 3' ends of RNA molecules, including mRNAs and small RNAs. This uridylation activity typically marks transcripts for degradation and modulates miRNA biogenesis and activity. By promoting RNA decay and dampening miRNA-mediated gene silencing pathways, CID-1 could antagonize the activity of pro-longevity small RNAs (e.g., those in the DAF-16/FOXO or germline silencing pathways). Loss of CID-1 function in C. elegans has been associated with checkpoint and RNA surveillance defects, but its primary molecular role in uridylating and destabilizing RNA species suggests it acts to reduce the abundance of transcripts or small RNAs that would otherwise support longevity. The zinc ion binding and 4Fe-4S ferredoxin-type domain further support a catalytically active nucleotidyltransferase role rather than a structural one, reinforcing its function in post-transcriptional RNA regulation that tends to oppose longevity-promoting gene expression programs.
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 "anti_longevity" for cid-1, matching the ground truth. However, the mechanistic reasoning is speculative and largely incorrect. The model classifies the mechanism as "epigenetic_alterations," which is a poor fit for an RNA uridylyltransferase. The actual mechanism of cid-1 in longevity is more directly related to its role in RNA surveillance and checkpoint control (it was originally identified as a caffeine-induced death gene involved in the S-phase checkpoint), not primarily through miRNA biogenesis or dampening pro-longevity small RNA pathways as the model suggests. The reasoning is largely constructed post-hoc from the gene's known biochemical functions rather than from actual experimental evidence about its longevity role. The model's logic (CID-1 destabilizes pro-longevity transcripts) is plausible but not well-supported, and the "epigenetic_alterations" classification is inappropriate for a post-transcriptional RNA modifier. The confidence of 0.62 is reasonable given the uncertainty.
Raw API responses
solver
{
"reasoning": "CID-1 (cytoplasmic poly(U) polymerase) is a terminal RNA uridylyltransferase (TUTase) in C. elegans that adds uridine residues to the 3' ends of RNA molecules, including mRNAs and small RNAs. This uridylation activity typically marks transcripts for degradation and modulates miRNA biogenesis and activity. By promoting RNA decay and dampening miRNA-mediated gene silencing pathways, CID-1 could antagonize the activity of pro-longevity small RNAs (e.g., those in the DAF-16/FOXO or germline silencing pathways). Loss of CID-1 function in C. elegans has been associated with checkpoint and RNA surveillance defects, but its primary molecular role in uridylating and destabilizing RNA species suggests it acts to reduce the abundance of transcripts or small RNAs that would otherwise support longevity. The zinc ion binding and 4Fe-4S ferredoxin-type domain further support a catalytically active nucleotidyltransferase role rather than a structural one, reinforcing its function in post-transcriptional RNA regulation that tends to oppose longevity-promoting gene expression programs.",
"confidence": 0.62,
"key_pathways": [
"RNA uridylation and decay",
"miRNA biogenesis and small RNA regulation",
"post-transcriptional gene silencing"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted \"anti_longevity\" for cid-1, matching the ground truth. However, the mechanistic reasoning is speculative and largely incorrect. The model classifies the mechanism as \"epigenetic_alterations,\" which is a poor fit for an RNA uridylyltransferase. The actual mechanism of cid-1 in longevity is more directly related to its role in RNA surveillance and checkpoint control (it was originally identified as a caffeine-induced death gene involved in the S-phase checkpoint), not primarily through miRNA biogenesis or dampening pro-longevity small RNA pathways as the model suggests. The reasoning is largely constructed post-hoc from the gene's known biochemical functions rather than from actual experimental evidence about its longevity role. The model's logic (CID-1 destabilizes pro-longevity transcripts) is plausible but not well-supported, and the \"epigenetic_alterations\" classification is inappropriate for a post-transcriptional RNA modifier. The confidence of 0.62 is reasonable given the uncertainty.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": true,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}