cel-1
C. elegans
mRNA guanylyltransferase
What the model saw
Gene: cel-1 Organism: Caenorhabditis elegans Known functions: mRNA guanylyltransferase. ATP binding. catalytic activity. mRNA 5'-triphosphate monophosphatase activity. mRNA guanylyltransferase activity. polynucleotide 5'-phosphatase activity.
View unredacted entry
mRNA guanylyltransferase. ATP binding. catalytic activity. mRNA 5'-triphosphate monophosphatase activity. mRNA guanylyltransferase activity. polynucleotide 5'-phosphatase activity.
Solver output
cel-1 encodes the mRNA guanylyltransferase (mRNA capping enzyme) in C. elegans, responsible for adding the 5' 7-methylguanosine cap to nascent pre-mRNAs. This cap is essential for mRNA stability, efficient translation initiation, and protection from 5'-exonucleolytic degradation. Proper mRNA capping is a prerequisite for maintaining proteostasis, as it ensures accurate and efficient translation of the proteome. Loss of capping enzyme function would broadly impair gene expression and protein synthesis, disrupting cellular homeostasis and stress responses that are critical for longevity. Because the 5' cap also interfaces with the eIF4F translation initiation complex and mTOR-regulated cap-dependent translation, cel-1 activity is integral to the regulated protein synthesis pathways that modulate lifespan in C. elegans.
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 cel-1, but the mechanistic reasoning is largely speculative and generic. The model reasons from first principles about mRNA capping being essential for proteostasis and translation, but this is a general argument that would apply to any essential gene. The actual mechanism by which cel-1 promotes longevity in C. elegans (likely through specific RNAi or genetic studies showing lifespan extension) is not described. The model invokes the mTOR/eIF4F axis without specific evidence that this is the relevant pathway for cel-1's longevity effect. The reasoning is plausible but not grounded in actual experimental findings about cel-1's role in aging. The confidence of 0.62 is somewhat appropriate given the uncertainty, but the reasoning quality is poor - it's essentially a generic argument about why any essential mRNA processing gene might be pro-longevity.
Raw API responses
solver
{
"reasoning": "cel-1 encodes the mRNA guanylyltransferase (mRNA capping enzyme) in C. elegans, responsible for adding the 5' 7-methylguanosine cap to nascent pre-mRNAs. This cap is essential for mRNA stability, efficient translation initiation, and protection from 5'-exonucleolytic degradation. Proper mRNA capping is a prerequisite for maintaining proteostasis, as it ensures accurate and efficient translation of the proteome. Loss of capping enzyme function would broadly impair gene expression and protein synthesis, disrupting cellular homeostasis and stress responses that are critical for longevity. Because the 5' cap also interfaces with the eIF4F translation initiation complex and mTOR-regulated cap-dependent translation, cel-1 activity is integral to the regulated protein synthesis pathways that modulate lifespan in C. elegans.",
"confidence": 0.62,
"key_pathways": [
"mRNA 5' capping and stability",
"cap-dependent translation initiation (eIF4F/mTOR axis)",
"proteostasis via regulated mRNA translation"
],
"mechanism_class": "other",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for cel-1, but the mechanistic reasoning is largely speculative and generic. The model reasons from first principles about mRNA capping being essential for proteostasis and translation, but this is a general argument that would apply to any essential gene. The actual mechanism by which cel-1 promotes longevity in C. elegans (likely through specific RNAi or genetic studies showing lifespan extension) is not described. The model invokes the mTOR/eIF4F axis without specific evidence that this is the relevant pathway for cel-1's longevity effect. The reasoning is plausible but not grounded in actual experimental findings about cel-1's role in aging. The confidence of 0.62 is somewhat appropriate given the uncertainty, but the reasoning quality is poor - it's essentially a generic argument about why any essential mRNA processing gene might be pro-longevity.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": true,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}