A mixture of acetic acid, furfural, and phenol (AFP), three representative lignocellulose-derived inhibitors, significantly inhibited the growth and bioethanol production of Saccharomyces cerevisiae. In order to uncover the mechanisms behind the enhanced tolerance of an inhibitor-tolerant S. cerevisiae strain (T), we measured the plasma membrane properties, which significantly influence cellular adaptation to inhibitors, of T strain and its parental strain (P) with and without AFP treatment. We integrated data obtained from multi-statistics-assisted phospholipidomics and parallel transcriptomics by using LC-tandem MS and microarray analysis. With the AFP treatment, the transcriptional changes of fatty acid metabolic genes showed a strong correlation with the increase of fatty-acyl-chain length of phosphatidylcholine (PC) and phosphatidylinositol (PI). This suggests a possible compensatory mechanism to cope with the increase of plasma membrane permeability and fluidity in both strains. Moreover, the absence of phosphatidylserine (PS) and phosphatidylethanolamine (PE) species from the most variable phospholipid species group was a discriminative feature of the T strain. This resulted from the decrease of CHO1 and increase of CHO2 levels of the T strain upon AFP treatment. These novel findings reveal that the coordinated transcription and phospholipid composition changes contribute to the increased robustness of the T strain and highlight potential metabolic engineering targets for mutants with higher tolerance.
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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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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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Evidence ID | Analyze ID | File | Description |
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