lsm-7
C. elegans
U6 snRNA-associated Sm-like protein LSm7
What the model saw
Gene: lsm-7 Organism: Caenorhabditis elegans Known functions: U6 snRNA-associated Sm-like protein LSm7. RNA binding. protein binding.
View unredacted entry
U6 snRNA-associated Sm-like protein LSm7. RNA binding. protein binding.
Solver output
LSm7 is a core component of the LSm2-8 complex that associates with U6 snRNA and is essential for pre-mRNA splicing via the spliceosome. Accurate pre-mRNA splicing is required for proper gene expression and proteome integrity; disruption of splicing fidelity is increasingly linked to aging phenotypes in C. elegans and other organisms. Additionally, LSm proteins participate in mRNA decay and RNA processing pathways that regulate stress-response and longevity-related transcripts. Maintenance of RNA processing fidelity through the LSm complex supports the broader category of epigenetic/transcriptional regulation that underpins healthy aging. Loss of splicing regulators in C. elegans has been shown to shorten lifespan, suggesting the normal function of lsm-7 is pro-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 lsm-7. However, the mechanism classification as "epigenetic_alterations" is questionable — RNA splicing/processing is not typically classified as epigenetic. The reasoning about splicing fidelity and RNA processing is plausible but somewhat generic, and the model doesn't cite specific experimental evidence for lsm-7's role in C. elegans longevity. The confidence of 0.55 is appropriately modest. The core logic (loss of splicing regulators shortens lifespan → lsm-7 is pro-longevity) is reasonable but not strongly supported by specific mechanistic evidence. The mechanism class "epigenetic_alterations" is a misclassification for what is fundamentally an RNA processing/splicing function.
Raw API responses
solver
{
"reasoning": "LSm7 is a core component of the LSm2-8 complex that associates with U6 snRNA and is essential for pre-mRNA splicing via the spliceosome. Accurate pre-mRNA splicing is required for proper gene expression and proteome integrity; disruption of splicing fidelity is increasingly linked to aging phenotypes in C. elegans and other organisms. Additionally, LSm proteins participate in mRNA decay and RNA processing pathways that regulate stress-response and longevity-related transcripts. Maintenance of RNA processing fidelity through the LSm complex supports the broader category of epigenetic/transcriptional regulation that underpins healthy aging. Loss of splicing regulators in C. elegans has been shown to shorten lifespan, suggesting the normal function of lsm-7 is pro-longevity.",
"confidence": 0.55,
"key_pathways": [
"U6 snRNA/spliceosome assembly",
"pre-mRNA splicing fidelity",
"mRNA decay and RNA processing"
],
"mechanism_class": "epigenetic_alterations",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for lsm-7. However, the mechanism classification as \"epigenetic_alterations\" is questionable — RNA splicing/processing is not typically classified as epigenetic. The reasoning about splicing fidelity and RNA processing is plausible but somewhat generic, and the model doesn't cite specific experimental evidence for lsm-7's role in C. elegans longevity. The confidence of 0.55 is appropriately modest. The core logic (loss of splicing regulators shortens lifespan → lsm-7 is pro-longevity) is reasonable but not strongly supported by specific mechanistic evidence. The mechanism class \"epigenetic_alterations\" is a misclassification for what is fundamentally an RNA processing/splicing function.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": true,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}