The ACO1 gene, encoding mitochondrial aconitase of Saccharomyces cerevisiae, is required both for oxidative metabolism and for glutamate prototrophy. This gene is subject to catabolite repression; the ACOI mRNA level is further reduced when glutamate is supplied with glucose. To further explore regulation of ACOI expression, we have screened for mutations that reduce expression of an ACOI-lacZ fusion borne on a multicopy vector. We identified a gene required for wild-type expression of ACOI only under catabolite repression conditions. Sequencing of the corresponding cloned gene revealed that it is identical to RTG2 previously cloned as a pivotal gene in controlling interorganelle retrograde communication. Cells containing either the original rtg2-2 mutation or a null rtg2 allele are not petite but show a residual growth on minimum glucose medium with ammonium sulfate as the sole nitrogen source. This growth defect is partially restored by supplying aspartate or threonine, and fully with glutamate or proline supplement. Surprisingly, this phenotype is not observed on complete medium lacking either of these amino acids. In addition, a genetic analysis revealed an interaction between RTG2 and ASP5 (encoding aspartate amino transferase), thus supporting our hypothesis that RTG2 may be involved in the control of several anaplerotic pathways.

• PMID: 8913736
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Journal Article | Research Support, Non-U.S. Gov't

Authors

Vélot C, Haviernik P, Lauquin GJ

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