mxl-2
C. elegans
Max-like protein homolog 2
What the model saw
Gene: mxl-2 Organism: Caenorhabditis elegans Known functions: Max-like protein homolog 2. DNA-binding transcription factor activity, RNA polymerase II-specific. RNA polymerase II cis-regulatory region sequence-specific DNA binding. protein binding. protein dimerization activity.
View unredacted entry
Max-like protein homolog 2. DNA-binding transcription factor activity, RNA polymerase II-specific. RNA polymerase II cis-regulatory region sequence-specific DNA binding. protein binding. protein dimerization activity.
Solver output
MXL-2 is the C. elegans homolog of Mlx/Max-like protein, a member of the Myc/Max/Mad transcriptional network. In this network, Max-like proteins dimerize with Mondo/ChREBP-family partners (such as MML-1 in C. elegans) to form transcriptional complexes that sense and respond to glucose/carbohydrate availability, directly linking nutrient sensing to gene expression. The MML-1/MXL-2 heterodimer in C. elegans has been shown to act downstream of mTORC1 and in parallel with AMPK/DAF-16 pathways to regulate metabolic gene expression and lifespan. Loss of mxl-2 disrupts this nutrient-sensing transcriptional program, and studies indicate that MXL-2 activity is required for normal longevity responses, particularly under dietary restriction or reduced insulin/IGF-1 signaling. Its role as a sequence-specific RNA Pol II transcription factor and obligate dimerization partner positions it as a positive regulator of metabolic homeostasis that 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 correctly predicted pro_longevity for mxl-2. The mechanistic reasoning is well-grounded: MXL-2 is indeed the C. elegans Mlx/Max-like protein that forms a heterodimer with MML-1 (the Mondo/ChREBP homolog) to regulate nutrient-sensing transcription. The model correctly identifies the MML-1/MXL-2 complex and its role in mTORC1-related nutrient sensing pathways. The connection to longevity through this glucose-sensing transcriptional complex is accurate. The confidence of 0.62 is reasonable given the specificity of the gene. Minor note: the claim about dietary restriction and insulin/IGF-1 signaling connections could be slightly overstated, but the core mechanism is correct.
Raw API responses
solver
{
"reasoning": "MXL-2 is the C. elegans homolog of Mlx/Max-like protein, a member of the Myc/Max/Mad transcriptional network. In this network, Max-like proteins dimerize with Mondo/ChREBP-family partners (such as MML-1 in C. elegans) to form transcriptional complexes that sense and respond to glucose/carbohydrate availability, directly linking nutrient sensing to gene expression. The MML-1/MXL-2 heterodimer in C. elegans has been shown to act downstream of mTORC1 and in parallel with AMPK/DAF-16 pathways to regulate metabolic gene expression and lifespan. Loss of mxl-2 disrupts this nutrient-sensing transcriptional program, and studies indicate that MXL-2 activity is required for normal longevity responses, particularly under dietary restriction or reduced insulin/IGF-1 signaling. Its role as a sequence-specific RNA Pol II transcription factor and obligate dimerization partner positions it as a positive regulator of metabolic homeostasis that supports longevity.",
"confidence": 0.62,
"key_pathways": [
"MML-1/MXL-2 glucose-sensing transcriptional complex",
"mTORC1/nutrient sensing pathway",
"Insulin/IGF-1 signaling and DAF-16 axis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for mxl-2. The mechanistic reasoning is well-grounded: MXL-2 is indeed the C. elegans Mlx/Max-like protein that forms a heterodimer with MML-1 (the Mondo/ChREBP homolog) to regulate nutrient-sensing transcription. The model correctly identifies the MML-1/MXL-2 complex and its role in mTORC1-related nutrient sensing pathways. The connection to longevity through this glucose-sensing transcriptional complex is accurate. The confidence of 0.62 is reasonable given the specificity of the gene. Minor note: the claim about dietary restriction and insulin/IGF-1 signaling connections could be slightly overstated, but the core mechanism is correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}