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inx-14

C. elegans

Innexin-14

What the model saw

Gene: inx-14
Organism: Caenorhabditis elegans
Known functions: Innexin-14. gap junction channel activity. gap junction hemi-channel activity.
View unredacted entry
Innexin-14. gap junction channel activity. gap junction hemi-channel activity.

Solver output

Predicted influence
Pro-longevity
Confidence
55%
Mechanism
Altered intercellular communication
Reasoning

INX-14 is a C. elegans innexin that forms gap junction channels and hemichannels, enabling direct intercellular communication between cells. In C. elegans, gap junctions mediated by innexins (particularly INX-14) are known to coordinate systemic signaling, including the propagation of germline signals that influence somatic aging and the transmission of stress-response signals across tissues. Loss of gap junction communication can disrupt coordinated tissue homeostasis and inter-tissue signaling that supports longevity, such as the relay of insulin/IGF-1-like signaling cues or mitochondrial stress signals between the germline and soma. INX-14 specifically has been implicated in germline-to-soma communication that modulates lifespan, suggesting its normal function facilitates pro-longevity intercellular coordination. Disruption of this channel activity impairs the systemic integration of metabolic and stress signals, which is detrimental to organismal longevity.

Key pathways
gap junction-mediated intercellular communicationgermline-to-soma signalingsystemic stress response coordination
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
Confident wrong
Notes

The model predicted pro_longevity but the ground truth is anti_longevity. The model reasoned that INX-14 facilitates pro-longevity intercellular communication, so its loss would be detrimental. However, the ground truth indicates inx-14 is anti_longevity, meaning its normal function actually shortens lifespan (or its loss extends lifespan). The mechanistic reasoning is also incorrect - INX-14 gap junction activity appears to be detrimental to longevity rather than beneficial. The model's reasoning about germline-to-soma communication being pro-longevity via INX-14 is not supported by the actual data. The model had moderate confidence (0.55) but was still wrong in both the answer and the mechanism.

Raw API responses

solver

{
  "reasoning": "INX-14 is a C. elegans innexin that forms gap junction channels and hemichannels, enabling direct intercellular communication between cells. In C. elegans, gap junctions mediated by innexins (particularly INX-14) are known to coordinate systemic signaling, including the propagation of germline signals that influence somatic aging and the transmission of stress-response signals across tissues. Loss of gap junction communication can disrupt coordinated tissue homeostasis and inter-tissue signaling that supports longevity, such as the relay of insulin/IGF-1-like signaling cues or mitochondrial stress signals between the germline and soma. INX-14 specifically has been implicated in germline-to-soma communication that modulates lifespan, suggesting its normal function facilitates pro-longevity intercellular coordination. Disruption of this channel activity impairs the systemic integration of metabolic and stress signals, which is detrimental to organismal longevity.",
  "confidence": 0.55,
  "key_pathways": [
    "gap junction-mediated intercellular communication",
    "germline-to-soma signaling",
    "systemic stress response coordination"
  ],
  "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 reasoned that INX-14 facilitates pro-longevity intercellular communication, so its loss would be detrimental. However, the ground truth indicates inx-14 is anti_longevity, meaning its normal function actually shortens lifespan (or its loss extends lifespan). The mechanistic reasoning is also incorrect - INX-14 gap junction activity appears to be detrimental to longevity rather than beneficial. The model's reasoning about germline-to-soma communication being pro-longevity via INX-14 is not supported by the actual data. The model had moderate confidence (0.55) but was still wrong in both the answer and the mechanism.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}