rpl-7A
C. elegans
Large ribosomal subunit protein eL8
What the model saw
Gene: rpl-7A Organism: Caenorhabditis elegans Known functions: Large ribosomal subunit protein eL8. RNA binding. calmodulin binding.
View unredacted entry
Large ribosomal subunit protein eL8. RNA binding. calmodulin binding.
Solver output
rpl-7A encodes the large ribosomal subunit protein eL8 (60S), a core component of the translational machinery. In C. elegans, partial loss-of-function of large ribosomal subunit proteins (including multiple rpl genes) is well-established to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling output. The normal function of rpl-7A is to promote ribosome assembly and translational capacity, which sustains high anabolic activity downstream of nutrient-sensing pathways (TOR, IIS). Elevated translation driven by ribosomal proteins accelerates aging by increasing proteotoxic burden and suppressing stress-response programs. The calmodulin-binding activity may additionally link ribosomal function to calcium-dependent signaling, but the dominant aging-relevant role is its contribution to ribosome biogenesis and translational output. Therefore, the wild-type (pro-translation) function of rpl-7A opposes 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 anti_longevity for rpl-7A. The mechanistic reasoning is sound: ribosomal protein knockdown in C. elegans extends lifespan by reducing translation rates, meaning the wild-type function of rpl-7A promotes aging (anti-longevity). The model correctly identifies the TOR/translational control pathway as the key mechanism. The classification of "deregulated_nutrient_sensing" is a reasonable framing, though "translational control" might be more precise. The reasoning is well-articulated and consistent with the literature on ribosomal protein knockdowns in C. elegans. Confidence of 0.75 is appropriate given the general knowledge about RPL proteins in aging.
Raw API responses
solver
{
"reasoning": "rpl-7A encodes the large ribosomal subunit protein eL8 (60S), a core component of the translational machinery. In C. elegans, partial loss-of-function of large ribosomal subunit proteins (including multiple rpl genes) is well-established to extend lifespan by reducing global translation rates, which mimics dietary restriction and downregulates TOR/TORC1 signaling output. The normal function of rpl-7A is to promote ribosome assembly and translational capacity, which sustains high anabolic activity downstream of nutrient-sensing pathways (TOR, IIS). Elevated translation driven by ribosomal proteins accelerates aging by increasing proteotoxic burden and suppressing stress-response programs. The calmodulin-binding activity may additionally link ribosomal function to calcium-dependent signaling, but the dominant aging-relevant role is its contribution to ribosome biogenesis and translational output. Therefore, the wild-type (pro-translation) function of rpl-7A opposes longevity.",
"confidence": 0.75,
"key_pathways": [
"TOR/TORC1 nutrient sensing and translational control",
"60S ribosome biogenesis and global protein synthesis",
"dietary restriction mimicry via ribosomal protein reduction"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for rpl-7A. The mechanistic reasoning is sound: ribosomal protein knockdown in C. elegans extends lifespan by reducing translation rates, meaning the wild-type function of rpl-7A promotes aging (anti-longevity). The model correctly identifies the TOR/translational control pathway as the key mechanism. The classification of \"deregulated_nutrient_sensing\" is a reasonable framing, though \"translational control\" might be more precise. The reasoning is well-articulated and consistent with the literature on ribosomal protein knockdowns in C. elegans. Confidence of 0.75 is appropriate given the general knowledge about RPL proteins in aging.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}