Rae1
M. musculus
ribonucleic acid export 1
What the model saw
Gene: Rae1 Organism: Mus musculus Known functions: ribonucleic acid export 1. mRNA export factor. RNA binding. ubiquitin binding.
View unredacted entry
ribonucleic acid export 1. mRNA export factor. RNA binding. ubiquitin binding.
Solver output
RAE1 (RNA export 1) is a WD-repeat protein that functions as an mRNA export factor, facilitating the transport of mRNAs from the nucleus to the cytoplasm through the nuclear pore complex. Critically, RAE1 also interacts with the APC/C (Anaphase-Promoting Complex/Cyclosome) co-activator CDH1 and is involved in mitotic spindle assembly checkpoint regulation; haploinsufficiency of Rae1 in mice leads to mitotic checkpoint defects, aneuploidy, and chromosomal instability. Its ubiquitin-binding activity further implicates it in proteostatic and cell cycle regulatory pathways. Loss of RAE1 function promotes genomic instability through mitotic errors and impaired mRNA export, both of which are hallmarks associated with accelerated aging and reduced longevity. Therefore, normal RAE1 function acts to preserve genomic integrity and support proper gene expression, placing it in a pro-longevity role.
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 pro_longevity for Rae1 in Mus musculus. The mechanistic reasoning is well-grounded: RAE1 haploinsufficiency in mice is known to cause mitotic checkpoint defects, aneuploidy, and chromosomal instability, which are associated with accelerated aging phenotypes. The model correctly identifies the genomic instability pathway as the key mechanism, and also correctly notes RAE1's roles in mRNA export and ubiquitin binding. The reasoning is coherent and biologically accurate. Confidence of 0.62 is appropriately moderate given the specificity of the gene's role in aging research.
Raw API responses
solver
{
"reasoning": "RAE1 (RNA export 1) is a WD-repeat protein that functions as an mRNA export factor, facilitating the transport of mRNAs from the nucleus to the cytoplasm through the nuclear pore complex. Critically, RAE1 also interacts with the APC/C (Anaphase-Promoting Complex/Cyclosome) co-activator CDH1 and is involved in mitotic spindle assembly checkpoint regulation; haploinsufficiency of Rae1 in mice leads to mitotic checkpoint defects, aneuploidy, and chromosomal instability. Its ubiquitin-binding activity further implicates it in proteostatic and cell cycle regulatory pathways. Loss of RAE1 function promotes genomic instability through mitotic errors and impaired mRNA export, both of which are hallmarks associated with accelerated aging and reduced longevity. Therefore, normal RAE1 function acts to preserve genomic integrity and support proper gene expression, placing it in a pro-longevity role.",
"confidence": 0.62,
"key_pathways": [
"mRNA nuclear export via nuclear pore complex",
"APC/C-CDH1 mitotic spindle assembly checkpoint",
"ubiquitin-mediated proteostasis"
],
"mechanism_class": "genomic_instability",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for Rae1 in Mus musculus. The mechanistic reasoning is well-grounded: RAE1 haploinsufficiency in mice is known to cause mitotic checkpoint defects, aneuploidy, and chromosomal instability, which are associated with accelerated aging phenotypes. The model correctly identifies the genomic instability pathway as the key mechanism, and also correctly notes RAE1's roles in mRNA export and ubiquitin binding. The reasoning is coherent and biologically accurate. Confidence of 0.62 is appropriately moderate given the specificity of the gene's role in aging research.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}