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hrpa-1

C. elegans

Heterogeneous nuclear ribonucleoprotein A1

What the model saw

Gene: hrpa-1
Organism: Caenorhabditis elegans
Known functions: Heterogeneous nuclear ribonucleoprotein A1. RNA binding. mRNA 3'-UTR binding. nucleic acid binding.
View unredacted entry
Heterogeneous nuclear ribonucleoprotein A1. RNA binding. mRNA 3'-UTR binding. nucleic acid binding.

Solver output

Predicted influence
Pro-longevity
Confidence
52%
Mechanism
Epigenetic alterations
Reasoning

HRPA-1 is the C. elegans ortholog of mammalian hnRNP A1, an RNA-binding protein that regulates post-transcriptional gene expression by binding mRNA 3'-UTRs and modulating mRNA stability, splicing, and translation. In the context of aging, hnRNP-family proteins are known to regulate the expression of stress-response and longevity-associated transcripts, including those in the DAF-16/FOXO and heat-shock response pathways, through 3'-UTR interactions. Post-transcriptional regulation of mRNA stability is a key component of proteostasis and stress-response networks that support longevity in C. elegans. Loss of such RNA-binding regulators can impair the proper expression of protective genes, suggesting a pro-longevity role. However, the specific targets of hrpa-1 in C. elegans are not fully characterized, introducing some uncertainty.

Key pathways
mRNA 3'-UTR post-transcriptional regulationDAF-16/FOXO stress-response pathwayRNA splicing and mRNA stability
Longevity influence
Anti-longevity
Lifespan effect
Increase

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

Answer
Incorrect
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Confident wrong
Notes

The model predicted pro_longevity while the ground truth is anti_longevity. The model's reasoning is generic and speculative, invoking DAF-16/FOXO pathways without specific evidence for hrpa-1. The model correctly identifies hrpa-1 as an RNA-binding protein involved in post-transcriptional regulation, but incorrectly infers a pro-longevity role. In reality, hrpa-1 is anti-longevity, meaning its loss likely extends lifespan. The model's logic (loss of RNA-binding regulators impairs protective gene expression → pro-longevity) is the opposite of what the data shows. The confidence of 0.52 is low but still leans wrong. The mechanism class of "epigenetic_alterations" is also questionable for an RNA-binding protein involved in post-transcriptional regulation.

Raw API responses

solver

{
  "reasoning": "HRPA-1 is the C. elegans ortholog of mammalian hnRNP A1, an RNA-binding protein that regulates post-transcriptional gene expression by binding mRNA 3'-UTRs and modulating mRNA stability, splicing, and translation. In the context of aging, hnRNP-family proteins are known to regulate the expression of stress-response and longevity-associated transcripts, including those in the DAF-16/FOXO and heat-shock response pathways, through 3'-UTR interactions. Post-transcriptional regulation of mRNA stability is a key component of proteostasis and stress-response networks that support longevity in C. elegans. Loss of such RNA-binding regulators can impair the proper expression of protective genes, suggesting a pro-longevity role. However, the specific targets of hrpa-1 in C. elegans are not fully characterized, introducing some uncertainty.",
  "confidence": 0.52,
  "key_pathways": [
    "mRNA 3'-UTR post-transcriptional regulation",
    "DAF-16/FOXO stress-response pathway",
    "RNA splicing and mRNA stability"
  ],
  "mechanism_class": "epigenetic_alterations",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model predicted pro_longevity while the ground truth is anti_longevity. The model's reasoning is generic and speculative, invoking DAF-16/FOXO pathways without specific evidence for hrpa-1. The model correctly identifies hrpa-1 as an RNA-binding protein involved in post-transcriptional regulation, but incorrectly infers a pro-longevity role. In reality, hrpa-1 is anti-longevity, meaning its loss likely extends lifespan. The model's logic (loss of RNA-binding regulators impairs protective gene expression → pro-longevity) is the opposite of what the data shows. The confidence of 0.52 is low but still leans wrong. The mechanism class of \"epigenetic_alterations\" is also questionable for an RNA-binding protein involved in post-transcriptional regulation.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}
hrpa-1 · Caenorhabditis elegans | Aging biology eval