← Browse entries

ifp-1

C. elegans

Intermediate filament protein ifp-1

What the model saw

Gene: ifp-1
Organism: Caenorhabditis elegans
Known functions: Intermediate filament protein ifp-1. structural constituent of cytoskeleton.
View unredacted entry
Intermediate filament protein ifp-1. structural constituent of cytoskeleton.

Solver output

Predicted influence
Unclear
Confidence
35%
Mechanism
Other
Reasoning

ifp-1 encodes an intermediate filament protein in C. elegans whose primary annotated function is as a structural constituent of the cytoskeleton. Intermediate filaments provide mechanical integrity to cells, but this structural role alone does not map cleanly onto a pro- or anti-longevity mechanism. While cytoskeletal integrity can influence cellular senescence and stem cell function, intermediate filaments in C. elegans (such as IFB-2 in the intestine) have context-dependent roles that are not straightforwardly linked to lifespan extension or reduction. Without additional functional data connecting ifp-1 to a specific aging pathway—such as proteostasis, nutrient sensing, or stress response—the annotation is too general to confidently assign a longevity direction.

Key pathways
intermediate filament cytoskeleton assemblymechanical cell integritycytoskeletal organization
Longevity influence
Anti-longevity
Lifespan effect
Increase

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
2/5
Failure mode
Appropriately uncertain
Notes

The model predicted "unclear" while the ground truth is "anti_longevity." The model's reasoning is plausible given the limited information provided (only structural cytoskeletal function annotated), but it failed to commit to the correct answer. The model appropriately acknowledged uncertainty but was unable to identify the anti-longevity role of ifp-1. No mechanistic reasoning about why ifp-1 would be anti-longevity was provided, so mechanism correctness cannot be confirmed. The model's reasoning quality is modest - it correctly identifies the lack of clear pathway connections but doesn't explore possibilities like cytoskeletal stiffness contributing to aging phenotypes or other mechanisms by which intermediate filament proteins could be anti-longevity.

Raw API responses

solver

{
  "reasoning": "ifp-1 encodes an intermediate filament protein in C. elegans whose primary annotated function is as a structural constituent of the cytoskeleton. Intermediate filaments provide mechanical integrity to cells, but this structural role alone does not map cleanly onto a pro- or anti-longevity mechanism. While cytoskeletal integrity can influence cellular senescence and stem cell function, intermediate filaments in C. elegans (such as IFB-2 in the intestine) have context-dependent roles that are not straightforwardly linked to lifespan extension or reduction. Without additional functional data connecting ifp-1 to a specific aging pathway—such as proteostasis, nutrient sensing, or stress response—the annotation is too general to confidently assign a longevity direction.",
  "confidence": 0.35,
  "key_pathways": [
    "intermediate filament cytoskeleton assembly",
    "mechanical cell integrity",
    "cytoskeletal organization"
  ],
  "mechanism_class": "other",
  "longevity_influence": "unclear"
}

advisor

{
  "notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity.\" The model's reasoning is plausible given the limited information provided (only structural cytoskeletal function annotated), but it failed to commit to the correct answer. The model appropriately acknowledged uncertainty but was unable to identify the anti-longevity role of ifp-1. No mechanistic reasoning about why ifp-1 would be anti-longevity was provided, so mechanism correctness cannot be confirmed. The model's reasoning quality is modest - it correctly identifies the lack of clear pathway connections but doesn't explore possibilities like cytoskeletal stiffness contributing to aging phenotypes or other mechanisms by which intermediate filament proteins could be anti-longevity.",
  "failure_mode": "appropriately_uncertain",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}