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spe-26

C. elegans

Spermatocyte protein spe-26

What the model saw

Gene: spe-26
Organism: Caenorhabditis elegans
Known functions: Spermatocyte protein spe-26. ubiquitin-like ligase-substrate adaptor activity.
View unredacted entry
Spermatocyte protein spe-26. ubiquitin-like ligase-substrate adaptor activity.

Solver output

Predicted influence
Unclear
Confidence
35%
Mechanism
Loss of proteostasis
Reasoning

SPE-26 is a spermatocyte-specific protein in C. elegans with ubiquitin-like ligase-substrate adaptor activity, meaning it recruits substrates to ubiquitin E3 ligase complexes for targeted degradation. While ubiquitin-mediated proteolysis is a key component of proteostasis and can influence longevity, SPE-26's function appears restricted to spermatogenesis, limiting its direct role in somatic aging pathways. In C. elegans, germline signals (including sperm vs. oocyte fate) can influence lifespan through DAF-16/FOXO and other pathways, but the specific substrate-adaptor role of SPE-26 in spermatocytes does not clearly map to a pro- or anti-longevity mechanism. The tissue-restricted expression and lack of known somatic targets make it difficult to assign a definitive longevity direction.

Key pathways
ubiquitin-proteasome systemspermatogenesisgermline signaling
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 "unclear" while the ground truth is "anti_longevity." In C. elegans, spe-26 loss-of-function mutations result in sterility (sperm defects), and sterile/germline-deficient worms often live longer due to germline signaling pathways (DAF-16/FOXO, DAF-2/insulin). The model actually touched on germline signaling as a key pathway but failed to connect the dots: loss of spe-26 → sperm defects/sterility → reduced germline proliferation signals → extended lifespan (anti_longevity means the gene normally suppresses longevity, so its loss extends life). The model's reasoning about tissue-restricted expression being a barrier to longevity influence was incorrect given the well-established germline-to-soma signaling in C. elegans lifespan regulation. The model was appropriately uncertain (confidence 0.35) but still got the answer wrong and missed the key mechanistic connection.

Raw API responses

solver

{
  "reasoning": "SPE-26 is a spermatocyte-specific protein in C. elegans with ubiquitin-like ligase-substrate adaptor activity, meaning it recruits substrates to ubiquitin E3 ligase complexes for targeted degradation. While ubiquitin-mediated proteolysis is a key component of proteostasis and can influence longevity, SPE-26's function appears restricted to spermatogenesis, limiting its direct role in somatic aging pathways. In C. elegans, germline signals (including sperm vs. oocyte fate) can influence lifespan through DAF-16/FOXO and other pathways, but the specific substrate-adaptor role of SPE-26 in spermatocytes does not clearly map to a pro- or anti-longevity mechanism. The tissue-restricted expression and lack of known somatic targets make it difficult to assign a definitive longevity direction.",
  "confidence": 0.35,
  "key_pathways": [
    "ubiquitin-proteasome system",
    "spermatogenesis",
    "germline signaling"
  ],
  "mechanism_class": "loss_of_proteostasis",
  "longevity_influence": "unclear"
}

advisor

{
  "notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity.\" In C. elegans, spe-26 loss-of-function mutations result in sterility (sperm defects), and sterile/germline-deficient worms often live longer due to germline signaling pathways (DAF-16/FOXO, DAF-2/insulin). The model actually touched on germline signaling as a key pathway but failed to connect the dots: loss of spe-26 → sperm defects/sterility → reduced germline proliferation signals → extended lifespan (anti_longevity means the gene normally suppresses longevity, so its loss extends life). The model's reasoning about tissue-restricted expression being a barrier to longevity influence was incorrect given the well-established germline-to-soma signaling in C. elegans lifespan regulation. The model was appropriately uncertain (confidence 0.35) but still got the answer wrong and missed the key mechanistic connection.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}