ccr-4
C. elegans
poly(A)-specific ribonuclease
What the model saw
Gene: ccr-4 Organism: Caenorhabditis elegans Known functions: poly(A)-specific ribonuclease. 3'-5'-RNA exonuclease activity. catalytic activity. poly(A)-specific ribonuclease activity.
View unredacted entry
poly(A)-specific ribonuclease. 3'-5'-RNA exonuclease activity. catalytic activity. poly(A)-specific ribonuclease activity.
Solver output
CCR-4 is the catalytic subunit of the CCR4-NOT deadenylase complex, which shortens poly(A) tails of mRNAs to trigger their decay. By controlling mRNA stability and turnover, CCR-4 acts as a post-transcriptional regulator of gene expression. In C. elegans, the CCR4-NOT complex has been linked to regulation of germline and somatic gene expression programs; deadenylation-mediated mRNA decay is a key mechanism for silencing pro-aging transcripts and maintaining translational fidelity. Loss of deadenylase activity can lead to aberrant stabilization of mRNAs encoding growth-promoting or stress-response-impairing factors, disrupting proteostasis and nutrient-sensing pathways. Additionally, CCR4-NOT-mediated deadenylation intersects with the DAF-16/FOXO and insulin/IGF-1 signaling axes in worms, where proper mRNA turnover supports longevity-associated transcriptional programs. The net effect of normal CCR-4 function is therefore to promote appropriate post-transcriptional gene regulation, supporting 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 ccr-4. However, the mechanism is classified as "epigenetic_alterations," which is not accurate for a poly(A)-specific ribonuclease/deadenylase — this is a post-transcriptional/mRNA decay mechanism, not an epigenetic one. The reasoning text itself is more reasonable (discussing mRNA deadenylation and decay), but the mechanism_class label is wrong. Additionally, the specific claim that CCR4-NOT intersects with DAF-16/FOXO and insulin/IGF-1 signaling in C. elegans in the way described appears to be somewhat speculative/hallucinated specifics rather than well-established literature. The reasoning is plausible but not strongly grounded in specific experimental evidence for ccr-4 in C. elegans longevity.
Raw API responses
solver
{
"reasoning": "CCR-4 is the catalytic subunit of the CCR4-NOT deadenylase complex, which shortens poly(A) tails of mRNAs to trigger their decay. By controlling mRNA stability and turnover, CCR-4 acts as a post-transcriptional regulator of gene expression. In C. elegans, the CCR4-NOT complex has been linked to regulation of germline and somatic gene expression programs; deadenylation-mediated mRNA decay is a key mechanism for silencing pro-aging transcripts and maintaining translational fidelity. Loss of deadenylase activity can lead to aberrant stabilization of mRNAs encoding growth-promoting or stress-response-impairing factors, disrupting proteostasis and nutrient-sensing pathways. Additionally, CCR4-NOT-mediated deadenylation intersects with the DAF-16/FOXO and insulin/IGF-1 signaling axes in worms, where proper mRNA turnover supports longevity-associated transcriptional programs. The net effect of normal CCR-4 function is therefore to promote appropriate post-transcriptional gene regulation, supporting longevity.",
"confidence": 0.62,
"key_pathways": [
"CCR4-NOT mRNA deadenylation and decay",
"post-transcriptional regulation of DAF-16/FOXO targets",
"mRNA stability control in insulin/IGF-1 signaling"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for ccr-4. However, the mechanism is classified as \"epigenetic_alterations,\" which is not accurate for a poly(A)-specific ribonuclease/deadenylase — this is a post-transcriptional/mRNA decay mechanism, not an epigenetic one. The reasoning text itself is more reasonable (discussing mRNA deadenylation and decay), but the mechanism_class label is wrong. Additionally, the specific claim that CCR4-NOT intersects with DAF-16/FOXO and insulin/IGF-1 signaling in C. elegans in the way described appears to be somewhat speculative/hallucinated specifics rather than well-established literature. The reasoning is plausible but not strongly grounded in specific experimental evidence for ccr-4 in C. elegans longevity.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": true,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}