A mutant was isolated that failed to derepress the 5' upstream region of Candida tropicalis isocitrate lyase gene (UPR-ICL)-mediated gene expression in acetate medium, and the gene (FIL1) that complemented this mutation was isolated. The fil1 null mutant in which FIL1 is disrupted (deltafil1 strain) could not grow on acetate or ethanol, and the derepression of the isocitrate lyase encoded by ICL1 in Saccharomyces cerevisiae was also defected. The amino acid sequence of Fil1p (230 amino acids) showed similarity to ribosome recycling factors (RRFs) of prokaryotes. Compared to prokaryotic RRFs, Fil1p had an N-terminal 46-amino-acid extension which was shown to be able to function as a mitochondrial-targeting sequence. The subcellular fractionation of the deltafil1 strain showed that protein constituents of the mitochondrial fraction of the deltafil1 strain differed from those of the wild-type strain, but resembled those of chloramphenicol-treated cells or rho(o) cells. The specific activity of cytochrome c oxidase, was severely decreased in deltafil1, rho(o) and chloramphenicol-treated cells compared with wild-type cells, while enzymatic levels of mitochondrial NAD+-linked isocitrate dehydrogenase, which is encoded by nuclear DNA, were not affected. These results suggest that Fillp is necessary for protein synthesis in mitochondria of S. cerevisiae. Furthermore, cells treated with antimycin A, along with chloramphenicol-treated, rho(o), and deltafil1 cells, showed deficiency in derepression of isocitrate lyase. Northern-blot analysis showed that this can be ascribed to no increase in transcription of ICL1 and FBP1 encoding fructose 1,6-bisphosphatase. The results indicate the presence of a communication pathway between mitochondria and the nucleus which represses expression of genes encoding the key enzymes of the glyoxylate cycle and gluconeogenic pathway when there is a deficiency in the mitochondrial respiratory chain.
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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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