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pat-3

C. elegans

Integrin beta pat-3

What the model saw

Gene: pat-3
Organism: Caenorhabditis elegans
Known functions: Integrin beta pat-3. integrin binding. protein binding.
View unredacted entry
Integrin beta pat-3. integrin binding. protein binding.

Solver output

Predicted influence
Unclear
Confidence
42%
Mechanism
Altered intercellular communication
Reasoning

pat-3 encodes the sole C. elegans integrin beta subunit, which heterodimerizes with alpha subunits (ina-1 or pat-2) to form transmembrane receptors that mediate cell-extracellular matrix adhesion and outside-in signaling. Integrins transduce mechanical and biochemical signals from the ECM to intracellular pathways including FAK/ILK, MAPK, and PI3K cascades, which can intersect with both pro-longevity (e.g., DAF-16/FOXO regulation) and pro-growth/anti-longevity signaling. While integrin-ECM communication is essential for tissue integrity and stem cell niche maintenance, loss of pat-3 is lethal (paralyzed arrested elongation at two-fold), making it difficult to assign a net longevity direction. The dual role of integrin signaling—supporting tissue homeostasis (pro-longevity) while also activating growth-promoting PI3K/Akt pathways (potentially anti-longevity)—creates genuine mechanistic conflict that prevents a clear directional prediction.

Key pathways
integrin-ECM adhesion signalingILK/FAK downstream signalingPI3K-Akt/DAF-16 pathway intersection
Longevity influence
Pro-longevity
Lifespan effect
Decrease

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

Answer
Incorrect
Mechanism
Incorrect
Reasoning quality
3/5
Failure mode
Appropriately uncertain
Notes

The model predicted "unclear" while the ground truth is "pro_longevity." The model's reasoning is thoughtful and acknowledges the lethality of pat-3 loss-of-function, the dual roles of integrin signaling, and the mechanistic conflicts. However, it failed to arrive at the correct directional answer. The model correctly identified key pathways (integrin-ECM, ILK/FAK, PI3K-Akt/DAF-16) but used the lethality of null mutants as a reason to avoid committing to a direction, rather than recognizing that partial loss or gain-of-function studies, or the role of integrin signaling in tissue homeostasis, would point toward pro-longevity. The reasoning quality is moderate — it's well-structured but ultimately leads to the wrong conclusion. The model's uncertainty was somewhat appropriate given the complexity, but the ground truth is clearly pro_longevity, so the prediction is incorrect.

Raw API responses

solver

{
  "reasoning": "pat-3 encodes the sole C. elegans integrin beta subunit, which heterodimerizes with alpha subunits (ina-1 or pat-2) to form transmembrane receptors that mediate cell-extracellular matrix adhesion and outside-in signaling. Integrins transduce mechanical and biochemical signals from the ECM to intracellular pathways including FAK/ILK, MAPK, and PI3K cascades, which can intersect with both pro-longevity (e.g., DAF-16/FOXO regulation) and pro-growth/anti-longevity signaling. While integrin-ECM communication is essential for tissue integrity and stem cell niche maintenance, loss of pat-3 is lethal (paralyzed arrested elongation at two-fold), making it difficult to assign a net longevity direction. The dual role of integrin signaling—supporting tissue homeostasis (pro-longevity) while also activating growth-promoting PI3K/Akt pathways (potentially anti-longevity)—creates genuine mechanistic conflict that prevents a clear directional prediction.",
  "confidence": 0.42,
  "key_pathways": [
    "integrin-ECM adhesion signaling",
    "ILK/FAK downstream signaling",
    "PI3K-Akt/DAF-16 pathway intersection"
  ],
  "mechanism_class": "altered_intercellular_communication",
  "longevity_influence": "unclear"
}

advisor

{
  "notes": "The model predicted \"unclear\" while the ground truth is \"pro_longevity.\" The model's reasoning is thoughtful and acknowledges the lethality of pat-3 loss-of-function, the dual roles of integrin signaling, and the mechanistic conflicts. However, it failed to arrive at the correct directional answer. The model correctly identified key pathways (integrin-ECM, ILK/FAK, PI3K-Akt/DAF-16) but used the lethality of null mutants as a reason to avoid committing to a direction, rather than recognizing that partial loss or gain-of-function studies, or the role of integrin signaling in tissue homeostasis, would point toward pro-longevity. The reasoning quality is moderate — it's well-structured but ultimately leads to the wrong conclusion. The model's uncertainty was somewhat appropriate given the complexity, but the ground truth is clearly pro_longevity, so the prediction is incorrect.",
  "failure_mode": "appropriately_uncertain",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 3,
  "ground_truth_questionable": false
}
pat-3 · Caenorhabditis elegans | Aging biology eval