snrp-3
C. elegans
U1 small nuclear ribonucleoprotein C
What the model saw
Gene: snrp-3 Organism: Caenorhabditis elegans Known functions: U1 small nuclear ribonucleoprotein C. U1 snRNA binding. mRNA binding. nucleic acid binding. pre-mRNA 5'-splice site binding. zinc ion binding.
View unredacted entry
U1 small nuclear ribonucleoprotein C. U1 snRNA binding. mRNA binding. nucleic acid binding. pre-mRNA 5'-splice site binding. zinc ion binding.
Solver output
snrp-3 encodes the U1 snRNP C protein, a core component of the U1 small nuclear ribonucleoprotein complex that recognizes the pre-mRNA 5'-splice site during the earliest step of spliceosome assembly. Accurate pre-mRNA splicing is essential for maintaining the fidelity of the transcriptome; loss of splicing fidelity leads to aberrant isoforms, proteotoxic stress, and dysregulated gene expression programs. In C. elegans, multiple splicing factors have been shown to be required for normal lifespan, as splicing accuracy declines with age and contributes to proteostatic collapse. The zinc ion binding activity of U1-C is critical for its direct contact with the 5'-splice site GU dinucleotide, stabilizing the U1 snRNP–pre-mRNA interaction and ensuring correct exon definition. By maintaining transcriptomic integrity, snrp-3 supports proteostasis and proper expression of longevity-relevant genes (e.g., daf-16/FOXO targets). This places its primary mechanism closest to epigenetic/gene expression regulation, which in the López-Otín framework maps to epigenetic alterations (loss of transcriptional fidelity).
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 about snrp-3's role in splicing fidelity and proteostasis is plausible in general terms, but it led to the wrong conclusion. The model assumed that because splicing fidelity is important for longevity, snrp-3 must be pro-longevity. However, the actual finding is that snrp-3 is anti-longevity, meaning its knockdown/loss likely extends lifespan (as is common in C. elegans RNAi screens). The mechanism class of "epigenetic_alterations" is also questionable for a splicing factor - this would more accurately be classified as RNA processing or transcriptional regulation. The model showed moderate confidence (0.62) but was still wrong on the key prediction.
Raw API responses
solver
{
"reasoning": "snrp-3 encodes the U1 snRNP C protein, a core component of the U1 small nuclear ribonucleoprotein complex that recognizes the pre-mRNA 5'-splice site during the earliest step of spliceosome assembly. Accurate pre-mRNA splicing is essential for maintaining the fidelity of the transcriptome; loss of splicing fidelity leads to aberrant isoforms, proteotoxic stress, and dysregulated gene expression programs. In C. elegans, multiple splicing factors have been shown to be required for normal lifespan, as splicing accuracy declines with age and contributes to proteostatic collapse. The zinc ion binding activity of U1-C is critical for its direct contact with the 5'-splice site GU dinucleotide, stabilizing the U1 snRNP–pre-mRNA interaction and ensuring correct exon definition. By maintaining transcriptomic integrity, snrp-3 supports proteostasis and proper expression of longevity-relevant genes (e.g., daf-16/FOXO targets). This places its primary mechanism closest to epigenetic/gene expression regulation, which in the López-Otín framework maps to epigenetic alterations (loss of transcriptional fidelity).",
"confidence": 0.62,
"key_pathways": [
"U1 snRNP-mediated 5'-splice site recognition",
"pre-mRNA splicing / spliceosome assembly",
"transcriptome integrity and proteostasis maintenance"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning about snrp-3's role in splicing fidelity and proteostasis is plausible in general terms, but it led to the wrong conclusion. The model assumed that because splicing fidelity is important for longevity, snrp-3 must be pro-longevity. However, the actual finding is that snrp-3 is anti-longevity, meaning its knockdown/loss likely extends lifespan (as is common in C. elegans RNAi screens). The mechanism class of \"epigenetic_alterations\" is also questionable for a splicing factor - this would more accurately be classified as RNA processing or transcriptional regulation. The model showed moderate confidence (0.62) but was still wrong on the key prediction.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}