MIG1 and SNF1 are two key regulatory factors involved in glucose repression of Saccharomyces cerevisiae. To enhance simultaneous utilization of glucose and xylose by engineered S. cerevisiae, single and double deletion strains of MIG1 and SNF1 were constructed. Combining shake flask fermentations and transcriptome analysis by RNA-Seq, the mechanism of MIG1 and SNF1 hierarchically regulating differentially expressed genes that might affect simultaneous utilization of glucose and xylose were elucidated. MIG1 deletion did not show any significant effect on co-utilization of mixed sugars. SNF1 deletion facilitated xylose consumption in mixed sugars as well as co-utilization of glucose and xylose, which might be due to that the SNF1 deletion resulted in the de-repression of some genes under nitrogen catabolite repression, thereby favorable to the utilization of nitrogen nutrient. Further deletion of MIG1 gene in the SNF1 deletion strain resulted in the de-repression of more genes under nitrogen catabolite repression and up-regulation of genes involved in carbon central metabolism. Compared with wild type strain, the MIG1 and SNF1 double deletion strain could co-utilize glucose and xylose, and accelerate ethanol accumulation, although this strain consumed glucose faster and xylose slower. Taken together, the MIG1 and SNF1 deletions resulted in up-regulation of genes under nitrogen catabolite repression, which could be beneficial to simultaneous utilization of glucose and xylose. MIG1 and SNF1 might be involved in the hierarchical regulatory network of genes under nitrogen catabolite repression. Dissection of this regulatory network could provide further insights to new targets for improving co-utilization of glucose and xylose.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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