tbb-2
C. elegans
Tubulin beta-2 chain
What the model saw
Gene: tbb-2 Organism: Caenorhabditis elegans Known functions: Tubulin beta-2 chain. GTP binding. GTPase activity. structural constituent of cytoskeleton.
View unredacted entry
Tubulin beta-2 chain. GTP binding. GTPase activity. structural constituent of cytoskeleton.
Solver output
TBB-2 is a beta-tubulin subunit that polymerizes with alpha-tubulin to form microtubules, using GTP binding and hydrolysis to drive dynamic instability. Microtubules are essential for cell division, intracellular transport, and neuronal function, making them broadly required for organismal viability rather than specifically pro- or anti-longevity. While microtubule dynamics have been linked to aging contexts such as mitotic fidelity and autophagosome trafficking, beta-tubulin itself is a structural housekeeping component without a directional role in canonical longevity pathways (e.g., IIS, TOR, or mitochondrial signaling). Loss of tbb-2 in C. elegans causes embryonic lethality or severe developmental defects, reflecting its essential structural role rather than a specific aging modulation. The functional annotations do not provide sufficient evidence to assign a clear pro- or anti-longevity direction.
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 "unclear" with low confidence (0.35), but the ground truth is "anti_longevity." The model's reasoning that tbb-2 is a housekeeping structural component without directional longevity influence is incorrect. In C. elegans, tbb-2 has been shown to have an anti-longevity role, meaning its loss or reduction extends lifespan. The model correctly identified the structural/cytoskeletal role of tbb-2 but failed to recognize that microtubule dynamics (specifically beta-tubulin) can influence aging through mechanisms like proteostasis, autophagy, or other aging-related pathways in C. elegans. The model's reasoning about embryonic lethality is partially correct for strong loss-of-function, but partial reduction of tbb-2 can extend lifespan. The model was overly conservative in assigning "unclear" when there is established evidence for anti-longevity classification.
Raw API responses
solver
{
"reasoning": "TBB-2 is a beta-tubulin subunit that polymerizes with alpha-tubulin to form microtubules, using GTP binding and hydrolysis to drive dynamic instability. Microtubules are essential for cell division, intracellular transport, and neuronal function, making them broadly required for organismal viability rather than specifically pro- or anti-longevity. While microtubule dynamics have been linked to aging contexts such as mitotic fidelity and autophagosome trafficking, beta-tubulin itself is a structural housekeeping component without a directional role in canonical longevity pathways (e.g., IIS, TOR, or mitochondrial signaling). Loss of tbb-2 in C. elegans causes embryonic lethality or severe developmental defects, reflecting its essential structural role rather than a specific aging modulation. The functional annotations do not provide sufficient evidence to assign a clear pro- or anti-longevity direction.",
"confidence": 0.35,
"key_pathways": [
"microtubule dynamic instability",
"GTP hydrolysis-driven tubulin polymerization",
"cytoskeletal organization"
],
"mechanism_class": "other",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" with low confidence (0.35), but the ground truth is \"anti_longevity.\" The model's reasoning that tbb-2 is a housekeeping structural component without directional longevity influence is incorrect. In C. elegans, tbb-2 has been shown to have an anti-longevity role, meaning its loss or reduction extends lifespan. The model correctly identified the structural/cytoskeletal role of tbb-2 but failed to recognize that microtubule dynamics (specifically beta-tubulin) can influence aging through mechanisms like proteostasis, autophagy, or other aging-related pathways in C. elegans. The model's reasoning about embryonic lethality is partially correct for strong loss-of-function, but partial reduction of tbb-2 can extend lifespan. The model was overly conservative in assigning \"unclear\" when there is established evidence for anti-longevity classification.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}