dct-13
C. elegans
C3H1-type domain-containing protein
What the model saw
Gene: dct-13 Organism: Caenorhabditis elegans Known functions: C3H1-type domain-containing protein. mRNA 3'-UTR AU-rich region binding. mRNA binding. mRNA regulatory element binding translation repressor activity. metal ion binding. protein-RNA sequence-specific adaptor activity.
View unredacted entry
C3H1-type domain-containing protein. mRNA 3'-UTR AU-rich region binding. mRNA binding. mRNA regulatory element binding translation repressor activity. metal ion binding. protein-RNA sequence-specific adaptor activity.
Solver output
dct-13 encodes a C3H1-type zinc finger domain protein that binds AU-rich elements (AREs) in mRNA 3'-UTRs and acts as a translation repressor via protein-RNA sequence-specific adaptor activity. ARE-binding proteins that repress translation are classically associated with post-transcriptional dampening of growth- and stress-response mRNAs, a mechanism that overlaps with translational control downstream of nutrient-sensing pathways (e.g., TOR/IIS). In C. elegans, global translational repression is a well-established pro-longevity mechanism; reduced translation extends lifespan through multiple effectors including IFE-2 (eIF4E) and downstream targets. By selectively repressing translation of ARE-containing mRNAs—which often encode pro-growth or inflammatory factors—dct-13 likely mimics the beneficial effects of reduced translational output. The metal ion binding (zinc coordination) is consistent with structural integrity of the C3H1 RNA-binding domain rather than an independent catalytic function. This places dct-13 in the translational/nutrient-sensing axis rather than a purely proteostasis or genomic-instability pathway.
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 was plausible on the surface — translational repression via ARE-binding proteins can be pro-longevity — but it reached the wrong conclusion. The model assumed that because dct-13 represses translation of ARE-containing mRNAs, it would extend lifespan, but the actual data shows it is anti-longevity (meaning loss of dct-13 extends lifespan, or its presence shortens it). The mechanistic reasoning was speculative and ultimately incorrect. The model had moderate confidence (0.62) but was still wrong. The reasoning quality is low because it built an elaborate but ultimately incorrect mechanistic story without considering that the specific targets of dct-13 repression might include pro-longevity mRNAs (e.g., stress response factors), which would make dct-13 anti-longevity.
Raw API responses
solver
{
"reasoning": "dct-13 encodes a C3H1-type zinc finger domain protein that binds AU-rich elements (AREs) in mRNA 3'-UTRs and acts as a translation repressor via protein-RNA sequence-specific adaptor activity. ARE-binding proteins that repress translation are classically associated with post-transcriptional dampening of growth- and stress-response mRNAs, a mechanism that overlaps with translational control downstream of nutrient-sensing pathways (e.g., TOR/IIS). In C. elegans, global translational repression is a well-established pro-longevity mechanism; reduced translation extends lifespan through multiple effectors including IFE-2 (eIF4E) and downstream targets. By selectively repressing translation of ARE-containing mRNAs—which often encode pro-growth or inflammatory factors—dct-13 likely mimics the beneficial effects of reduced translational output. The metal ion binding (zinc coordination) is consistent with structural integrity of the C3H1 RNA-binding domain rather than an independent catalytic function. This places dct-13 in the translational/nutrient-sensing axis rather than a purely proteostasis or genomic-instability pathway.",
"confidence": 0.62,
"key_pathways": [
"mRNA 3'-UTR AU-rich element-mediated translational repression",
"TOR-dependent translational control",
"post-transcriptional gene regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning was plausible on the surface — translational repression via ARE-binding proteins can be pro-longevity — but it reached the wrong conclusion. The model assumed that because dct-13 represses translation of ARE-containing mRNAs, it would extend lifespan, but the actual data shows it is anti-longevity (meaning loss of dct-13 extends lifespan, or its presence shortens it). The mechanistic reasoning was speculative and ultimately incorrect. The model had moderate confidence (0.62) but was still wrong. The reasoning quality is low because it built an elaborate but ultimately incorrect mechanistic story without considering that the specific targets of dct-13 repression might include pro-longevity mRNAs (e.g., stress response factors), which would make dct-13 anti-longevity.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}