RAD55
S. cerevisiae
putative DNA-dependent ATPase RAD55
What the model saw
Gene: RAD55 Organism: Saccharomyces cerevisiae Known functions: putative DNA-dependent ATPase RAD55. ATP binding. ATP-dependent DNA damage sensor activity. ATP-dependent activity, acting on DNA. DNA binding. crossover junction DNA endonuclease activity. four-way junction DNA binding. protein binding.
View unredacted entry
putative DNA-dependent ATPase RAD55. ATP binding. ATP-dependent DNA damage sensor activity. ATP-dependent activity, acting on DNA. DNA binding. crossover junction DNA endonuclease activity. four-way junction DNA binding. protein binding.
Solver output
RAD55 is a RecA/Rad51 paralog in S. cerevisiae that functions in homologous recombination (HR)-mediated DNA repair. Its ATP-dependent DNA damage sensor activity and four-way (Holliday) junction DNA binding indicate a direct role in recognizing and processing DNA double-strand breaks and stalled replication forks. By facilitating Rad51 filament assembly and stabilization on ssDNA, RAD55 promotes accurate HR repair, reducing the accumulation of mutations and chromosomal rearrangements. The crossover junction endonuclease activity further supports resolution of recombination intermediates, ensuring genome integrity. Loss of RAD55 function leads to increased DNA damage sensitivity and elevated mutation rates, hallmarks of genomic instability that accelerate aging; thus its normal function opposes genomic instability and supports longevity.
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 pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — RAD55 does function in homologous recombination and DNA repair — but it drew the wrong conclusion about longevity influence. In yeast, RAD55 (and related HR factors) can actually promote recombination events that lead to loss of heterozygosity or other genomic rearrangements that shorten lifespan, making it anti-longevity. The model's mechanistic framing (that DNA repair genes are always pro-longevity) is an oversimplification. The model was fairly confident (0.75) in the wrong direction. The mechanism described (HR repair, Rad51 filament assembly) is partially correct in terms of RAD55's biochemical function, but the interpretation of its effect on longevity is wrong.
Raw API responses
solver
{
"reasoning": "RAD55 is a RecA/Rad51 paralog in S. cerevisiae that functions in homologous recombination (HR)-mediated DNA repair. Its ATP-dependent DNA damage sensor activity and four-way (Holliday) junction DNA binding indicate a direct role in recognizing and processing DNA double-strand breaks and stalled replication forks. By facilitating Rad51 filament assembly and stabilization on ssDNA, RAD55 promotes accurate HR repair, reducing the accumulation of mutations and chromosomal rearrangements. The crossover junction endonuclease activity further supports resolution of recombination intermediates, ensuring genome integrity. Loss of RAD55 function leads to increased DNA damage sensitivity and elevated mutation rates, hallmarks of genomic instability that accelerate aging; thus its normal function opposes genomic instability and supports longevity.",
"confidence": 0.75,
"key_pathways": [
"homologous recombination DNA repair",
"Rad51 filament assembly and stabilization",
"Holliday junction resolution"
],
"mechanism_class": "genomic_instability",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible on the surface — RAD55 does function in homologous recombination and DNA repair — but it drew the wrong conclusion about longevity influence. In yeast, RAD55 (and related HR factors) can actually promote recombination events that lead to loss of heterozygosity or other genomic rearrangements that shorten lifespan, making it anti-longevity. The model's mechanistic framing (that DNA repair genes are always pro-longevity) is an oversimplification. The model was fairly confident (0.75) in the wrong direction. The mechanism described (HR repair, Rad51 filament assembly) is partially correct in terms of RAD55's biochemical function, but the interpretation of its effect on longevity is wrong.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}