SGS1
S. cerevisiae
ATP-dependent DNA helicase SGS1
What the model saw
Gene: SGS1 Organism: Saccharomyces cerevisiae Known functions: ATP-dependent DNA helicase SGS1. 3'-5' DNA helicase activity. ATP binding. ATP hydrolysis activity. DNA helicase activity. DNA topoisomerase binding. four-way junction helicase activity. helicase activity. nucleic acid binding. nucleotide binding. protein binding. zinc ion binding.
View unredacted entry
ATP-dependent DNA helicase SGS1. 3'-5' DNA helicase activity. ATP binding. ATP hydrolysis activity. DNA helicase activity. DNA topoisomerase binding. four-way junction helicase activity. helicase activity. nucleic acid binding. nucleotide binding. protein binding. zinc ion binding.
Solver output
SGS1 is the sole RecQ-family DNA helicase in S. cerevisiae and is the ortholog of human BLM/WRN/RECQL4, mutations in which cause premature aging syndromes (Bloom, Werner, Rothmund-Thomson). Its 3'-5' ATP-dependent helicase activity, four-way (Holliday) junction unwinding, and DNA topoisomerase binding are essential for resolving stalled replication forks, suppressing aberrant recombination intermediates, and facilitating DNA double-strand break repair via homologous recombination. Loss of SGS1 leads to elevated gross chromosomal rearrangements, increased mitotic recombination, and accelerated replicative aging in yeast. By maintaining genome integrity during DNA replication and repair, SGS1 directly counteracts the accumulation of genomic instability that drives cellular aging and limits replicative lifespan.
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 correctly predicted SGS1 as pro_longevity with high confidence (0.92). The mechanistic reasoning is excellent: it correctly identifies SGS1 as the sole RecQ-family helicase in yeast, draws the appropriate parallel to human Werner/Bloom syndrome helicases, explains the role in resolving Holliday junctions, suppressing aberrant recombination, and maintaining genome integrity during replication. The key pathways listed (STR complex with Top3-Rmi1, HR/DSB repair) are accurate and well-supported by the literature. The connection between genomic instability and replicative aging in yeast is correctly articulated.
Raw API responses
solver
{
"reasoning": "SGS1 is the sole RecQ-family DNA helicase in S. cerevisiae and is the ortholog of human BLM/WRN/RECQL4, mutations in which cause premature aging syndromes (Bloom, Werner, Rothmund-Thomson). Its 3'-5' ATP-dependent helicase activity, four-way (Holliday) junction unwinding, and DNA topoisomerase binding are essential for resolving stalled replication forks, suppressing aberrant recombination intermediates, and facilitating DNA double-strand break repair via homologous recombination. Loss of SGS1 leads to elevated gross chromosomal rearrangements, increased mitotic recombination, and accelerated replicative aging in yeast. By maintaining genome integrity during DNA replication and repair, SGS1 directly counteracts the accumulation of genomic instability that drives cellular aging and limits replicative lifespan.",
"confidence": 0.92,
"key_pathways": [
"RecQ helicase / DNA repair and replication fork stabilization",
"Holliday junction dissolution (STR complex with Top3-Rmi1)",
"Homologous recombination / double-strand break repair"
],
"mechanism_class": "genomic_instability",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted SGS1 as pro_longevity with high confidence (0.92). The mechanistic reasoning is excellent: it correctly identifies SGS1 as the sole RecQ-family helicase in yeast, draws the appropriate parallel to human Werner/Bloom syndrome helicases, explains the role in resolving Holliday junctions, suppressing aberrant recombination, and maintaining genome integrity during replication. The key pathways listed (STR complex with Top3-Rmi1, HR/DSB repair) are accurate and well-supported by the literature. The connection between genomic instability and replicative aging in yeast is correctly articulated.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}