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ain-1

C. elegans

ALG-1 INteracting protein

What the model saw

Gene: ain-1
Organism: Caenorhabditis elegans
Known functions: ALG-1 INteracting protein. protein binding.
View unredacted entry
ALG-1 INteracting protein. protein binding.

Solver output

Predicted influence
Pro-longevity
Confidence
62%
Mechanism
Epigenetic alterations
Reasoning

AIN-1 is a GW182/TNRC6 ortholog in C. elegans that interacts with ALG-1, the Argonaute protein central to the miRNA-induced silencing complex (miRISC). AIN-1 functions as a scaffold within miRISC, bridging Argonaute-bound miRNAs to downstream effectors of translational repression and mRNA deadenylation. miRNA-mediated gene silencing via the ALG-1/AIN-1 complex is required for proper regulation of developmental timing and stress responses, including modulation of the DAF-2/insulin-IGF-1 signaling pathway through miRNAs such as miR-71 and let-7 family members. Loss of ain-1 disrupts miRISC function, impairing post-transcriptional silencing of pro-aging targets, and has been associated with reduced lifespan in C. elegans. Thus, the normal function of AIN-1 in supporting miRNA-mediated repression of aging-promoting transcripts is pro-longevity.

Key pathways
miRNA-induced silencing complex (miRISC)ALG-1/Argonaute-mediated post-transcriptional regulationDAF-2/insulin-IGF-1 signaling modulation via miRNAs
Longevity influence
Pro-longevity
Lifespan effect
Decrease

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
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted pro_longevity for ain-1. The mechanistic reasoning is well-grounded: AIN-1 is indeed a GW182/TNRC6 ortholog that functions within the miRISC complex alongside ALG-1, and miRNA-mediated silencing is known to influence longevity in C. elegans. The connection to DAF-2/insulin-IGF-1 signaling via miRNAs like miR-71 and let-7 family members is plausible and consistent with the literature. The classification as "epigenetic_alterations" is a slight stretch — miRNA-mediated post-transcriptional silencing is more accurately described as post-transcriptional regulation rather than epigenetic alteration in the strict sense, but this is a minor categorization issue. Overall, the reasoning is solid and the answer is correct.

Raw API responses

solver

{
  "reasoning": "AIN-1 is a GW182/TNRC6 ortholog in C. elegans that interacts with ALG-1, the Argonaute protein central to the miRNA-induced silencing complex (miRISC). AIN-1 functions as a scaffold within miRISC, bridging Argonaute-bound miRNAs to downstream effectors of translational repression and mRNA deadenylation. miRNA-mediated gene silencing via the ALG-1/AIN-1 complex is required for proper regulation of developmental timing and stress responses, including modulation of the DAF-2/insulin-IGF-1 signaling pathway through miRNAs such as miR-71 and let-7 family members. Loss of ain-1 disrupts miRISC function, impairing post-transcriptional silencing of pro-aging targets, and has been associated with reduced lifespan in C. elegans. Thus, the normal function of AIN-1 in supporting miRNA-mediated repression of aging-promoting transcripts is pro-longevity.",
  "confidence": 0.62,
  "key_pathways": [
    "miRNA-induced silencing complex (miRISC)",
    "ALG-1/Argonaute-mediated post-transcriptional regulation",
    "DAF-2/insulin-IGF-1 signaling modulation via miRNAs"
  ],
  "mechanism_class": "epigenetic_alterations",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for ain-1. The mechanistic reasoning is well-grounded: AIN-1 is indeed a GW182/TNRC6 ortholog that functions within the miRISC complex alongside ALG-1, and miRNA-mediated silencing is known to influence longevity in C. elegans. The connection to DAF-2/insulin-IGF-1 signaling via miRNAs like miR-71 and let-7 family members is plausible and consistent with the literature. The classification as \"epigenetic_alterations\" is a slight stretch — miRNA-mediated post-transcriptional silencing is more accurately described as post-transcriptional regulation rather than epigenetic alteration in the strict sense, but this is a minor categorization issue. Overall, the reasoning is solid and the answer is correct.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}