eef-1A.1
C. elegans
Elongation factor 1-alpha
What the model saw
Gene: eef-1A.1 Organism: Caenorhabditis elegans Known functions: Elongation factor 1-alpha. GTP binding. GTPase activity. translation elongation factor activity. translation factor activity, RNA binding.
View unredacted entry
Elongation factor 1-alpha. GTP binding. GTPase activity. translation elongation factor activity. translation factor activity, RNA binding.
Solver output
EEF-1A.1 encodes the elongation factor 1-alpha (eEF1A), which in its GTP-bound form delivers aminoacyl-tRNAs to the ribosomal A-site, directly driving translational elongation rate and overall protein synthesis output. Elevated or unrestrained global translation is a well-established driver of aging in C. elegans: partial knockdown of translation elongation factors (including eEF1A homologs) extends lifespan, consistent with the broader finding that reduced ribosomal and translational activity promotes longevity via improved proteostasis and reduced production of misfolded proteins. The GTPase cycle of eEF1A is central to elongation speed; high elongation activity increases the load of newly synthesized proteins that must be folded, raising the risk of proteotoxic stress. This places eEF-1A.1's normal function in opposition to longevity, acting through the proteostasis/translation axis rather than a nutrient-sensing pathway per se.
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 anti_longevity for eef-1A.1 in C. elegans. The mechanistic reasoning is sound and well-supported: eEF1A drives translational elongation, and reducing translation elongation factor activity is known to extend lifespan in C. elegans through improved proteostasis. The model correctly identifies that the gene's normal function (promoting translation) opposes longevity, making it anti_longevity. The confidence of 0.72 is appropriate given the well-established literature on translation and aging in C. elegans. The reasoning about proteostasis, translational load, and the GTPase cycle is accurate and detailed.
Raw API responses
solver
{
"reasoning": "EEF-1A.1 encodes the elongation factor 1-alpha (eEF1A), which in its GTP-bound form delivers aminoacyl-tRNAs to the ribosomal A-site, directly driving translational elongation rate and overall protein synthesis output. Elevated or unrestrained global translation is a well-established driver of aging in C. elegans: partial knockdown of translation elongation factors (including eEF1A homologs) extends lifespan, consistent with the broader finding that reduced ribosomal and translational activity promotes longevity via improved proteostasis and reduced production of misfolded proteins. The GTPase cycle of eEF1A is central to elongation speed; high elongation activity increases the load of newly synthesized proteins that must be folded, raising the risk of proteotoxic stress. This places eEF-1A.1's normal function in opposition to longevity, acting through the proteostasis/translation axis rather than a nutrient-sensing pathway per se.",
"confidence": 0.72,
"key_pathways": [
"translational elongation (eEF1A GTPase cycle)",
"proteostasis / protein quality control",
"ribosome-mediated lifespan regulation"
],
"mechanism_class": "loss_of_proteostasis",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for eef-1A.1 in C. elegans. The mechanistic reasoning is sound and well-supported: eEF1A drives translational elongation, and reducing translation elongation factor activity is known to extend lifespan in C. elegans through improved proteostasis. The model correctly identifies that the gene's normal function (promoting translation) opposes longevity, making it anti_longevity. The confidence of 0.72 is appropriate given the well-established literature on translation and aging in C. elegans. The reasoning about proteostasis, translational load, and the GTPase cycle is accurate and detailed.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}