sma-10
C. elegans
Leucine-rich repeats and immunoglobulin-like domains protein sma-10
What the model saw
Gene: sma-10 Organism: Caenorhabditis elegans Known functions: Leucine-rich repeats and immunoglobulin-like domains protein sma-10. signaling receptor activity. type I transforming growth factor beta receptor binding. type II transforming growth factor beta receptor binding.
View unredacted entry
Leucine-rich repeats and immunoglobulin-like domains protein sma-10. signaling receptor activity. type I transforming growth factor beta receptor binding. type II transforming growth factor beta receptor binding.
Solver output
SMA-10 is a leucine-rich repeat and immunoglobulin-like domain (LRIG) co-receptor that binds both type I and type II TGF-β receptors, functioning as a positive modulator of BMP/TGF-β signaling in C. elegans. In the worm, the BMP-like Sma/Mab pathway (through ligand DBL-1, receptors SMA-6/DAF-4, and downstream SMADs) promotes body size and has been linked to longevity regulation; sma-10 enhances signaling through this pathway by facilitating receptor complex assembly. Positive regulators of BMP signaling in C. elegans tend to be pro-longevity, as the Sma/Mab pathway intersects with stress response and body-size regulation that correlates with lifespan extension. Loss of sma-10 reduces BMP pathway output, phenocopying small-body mutants, which are generally associated with reduced, not extended, lifespan in this context. Thus, the normal function of sma-10—amplifying TGF-β/BMP receptor signaling—supports organismal homeostasis and intercellular communication in a manner consistent with promoting 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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning about sma-10 being a positive modulator of BMP/TGF-β signaling is partially correct mechanistically (sma-10 does act as a co-receptor enhancing BMP signaling), but the model incorrectly concluded that this makes it pro-longevity. In C. elegans, the Sma/Mab BMP pathway (DBL-1 pathway) actually has anti-longevity effects - activation of this pathway reduces lifespan, and loss-of-function mutations in this pathway (small body mutants) tend to be long-lived, not short-lived. The model made the opposite inference about the relationship between BMP signaling and longevity in C. elegans. The model was also fairly confident (0.72) in its wrong answer. The reasoning about small-body mutants being associated with reduced lifespan is incorrect - small body sma mutants are actually often long-lived in C. elegans.
Raw API responses
solver
{
"reasoning": "SMA-10 is a leucine-rich repeat and immunoglobulin-like domain (LRIG) co-receptor that binds both type I and type II TGF-β receptors, functioning as a positive modulator of BMP/TGF-β signaling in C. elegans. In the worm, the BMP-like Sma/Mab pathway (through ligand DBL-1, receptors SMA-6/DAF-4, and downstream SMADs) promotes body size and has been linked to longevity regulation; sma-10 enhances signaling through this pathway by facilitating receptor complex assembly. Positive regulators of BMP signaling in C. elegans tend to be pro-longevity, as the Sma/Mab pathway intersects with stress response and body-size regulation that correlates with lifespan extension. Loss of sma-10 reduces BMP pathway output, phenocopying small-body mutants, which are generally associated with reduced, not extended, lifespan in this context. Thus, the normal function of sma-10—amplifying TGF-β/BMP receptor signaling—supports organismal homeostasis and intercellular communication in a manner consistent with promoting longevity.",
"confidence": 0.72,
"key_pathways": [
"BMP/Sma-Mab TGF-β signaling pathway",
"SMA-6/DAF-4 receptor complex modulation",
"intercellular ligand-receptor communication"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning about sma-10 being a positive modulator of BMP/TGF-β signaling is partially correct mechanistically (sma-10 does act as a co-receptor enhancing BMP signaling), but the model incorrectly concluded that this makes it pro-longevity. In C. elegans, the Sma/Mab BMP pathway (DBL-1 pathway) actually has anti-longevity effects - activation of this pathway reduces lifespan, and loss-of-function mutations in this pathway (small body mutants) tend to be long-lived, not short-lived. The model made the opposite inference about the relationship between BMP signaling and longevity in C. elegans. The model was also fairly confident (0.72) in its wrong answer. The reasoning about small-body mutants being associated with reduced lifespan is incorrect - small body sma mutants are actually often long-lived in C. elegans.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}