mys
D. melanogaster
myospheroid
What the model saw
Gene: mys Organism: Drosophila melanogaster Known functions: myospheroid. extracellular matrix protein binding. integrin binding. protein binding. protein heterodimerization activity. transmembrane signaling receptor activity.
View unredacted entry
myospheroid. extracellular matrix protein binding. integrin binding. protein binding. protein heterodimerization activity. transmembrane signaling receptor activity.
Solver output
mys encodes the Drosophila βPS integrin subunit, which heterodimerizes with α-integrin subunits to form functional integrin receptors at the cell surface. Integrins mediate bidirectional signaling between cells and the extracellular matrix (ECM), engaging pathways such as FAK/Src and PI3K/Akt that regulate cell survival, tissue homeostasis, and stem cell niche maintenance. Proper integrin-ECM communication is essential for maintaining tissue integrity and stem cell function during aging; loss of integrin signaling leads to tissue degeneration, muscle detachment, and impaired stem cell niche interactions. In aging Drosophila, declining integrin-mediated adhesion contributes to muscle and gut epithelial deterioration, hallmarks of organismal aging. Therefore, normal mys function, by sustaining ECM-cell communication and tissue cohesion, is expected to be 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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — mys encodes βPS integrin, and integrin signaling does play roles in tissue homeostasis. However, the model assumed that because integrins support tissue integrity, mys must be pro-longevity. In reality, mys is classified as anti_longevity, meaning its normal activity reduces lifespan (e.g., loss-of-function or reduced expression may extend lifespan). The model failed to consider that integrin signaling can also promote aging-related processes, or that overactive integrin/ECM signaling could be detrimental to longevity. The reasoning quality is moderate — it's mechanistically coherent but reaches the wrong conclusion, and the model had moderate confidence (0.62) in the wrong direction.
Raw API responses
solver
{
"reasoning": "mys encodes the Drosophila βPS integrin subunit, which heterodimerizes with α-integrin subunits to form functional integrin receptors at the cell surface. Integrins mediate bidirectional signaling between cells and the extracellular matrix (ECM), engaging pathways such as FAK/Src and PI3K/Akt that regulate cell survival, tissue homeostasis, and stem cell niche maintenance. Proper integrin-ECM communication is essential for maintaining tissue integrity and stem cell function during aging; loss of integrin signaling leads to tissue degeneration, muscle detachment, and impaired stem cell niche interactions. In aging Drosophila, declining integrin-mediated adhesion contributes to muscle and gut epithelial deterioration, hallmarks of organismal aging. Therefore, normal mys function, by sustaining ECM-cell communication and tissue cohesion, is expected to be pro-longevity.",
"confidence": 0.62,
"key_pathways": [
"integrin-ECM signaling",
"FAK/Src/PI3K-Akt cell survival pathway",
"stem cell niche maintenance"
],
"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 is plausible on the surface — mys encodes βPS integrin, and integrin signaling does play roles in tissue homeostasis. However, the model assumed that because integrins support tissue integrity, mys must be pro-longevity. In reality, mys is classified as anti_longevity, meaning its normal activity reduces lifespan (e.g., loss-of-function or reduced expression may extend lifespan). The model failed to consider that integrin signaling can also promote aging-related processes, or that overactive integrin/ECM signaling could be detrimental to longevity. The reasoning quality is moderate — it's mechanistically coherent but reaches the wrong conclusion, and the model had moderate confidence (0.62) in the wrong direction.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}