Mig2 has been described as a transcriptional factor that in the absence of Mig1 protein is required for glucose repression of the SUC2 gene. Thus, until now, the main role assigned to Mig2 has been the functional redundancy to Mig1. In this study, we report that Mig2 has a double subcellular localization. As expected, in high-glucose conditions it is accumulated in the nucleus but in low-glucose conditions Mig2 has an unexpected mitochondrial localization and role in mitochondrial morphology. We describe that Mig2 physically interacts with the mitochondrial protein Ups1 in a glucose-dependent manner. We also show that ?mig2 mutant cells exhibit a fragmented network of mitochondrial tubules, a phenotype similarly observed in cells lacking Fzo1 and Ups1. Furthermore, Mig2 acts antagonistically with respect to the fission-promoting components, because mitochondrial aggregation induced by DNM1 deletion was rescued in the ?dnm1?mig2 double mutant. Thus, our studies have revealed an additional role for Mig2 as a novel factor required for the maintenance of fusion-competent mitochondria in Saccharomyces cerevisiae and strongly suggest that Mig2 could be involved in the cross talk between the nucleus and the mitochondria through Ups1 to regulate mitochondrial morphology in a glucose dependent manner.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Annotation Extension||Reference|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Assay||Construct||Conditions||Strain Background||Reference|