ArticleGenetics1996
The Saccharomyces cerevisiae RTG2 gene is a regulator of aconitase expression under catabolite repression conditions.
Article in Genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 31 citations in OpenAlex.
- Retrograde signaling mediates an adaptive survival response to endoplasmic reticulum stress inJournal of cell science · 2020Article
- Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes.Oxidative medicine and cellular longevity · 2015Review
- Mitochondrial DNA instability in cells lacking aconitase correlates with iron citrate toxicity.Oxidative medicine and cellular longevity · 2013Article
- Reactive oxygen species-mediated regulation of mitochondrial biogenesis in the yeast Saccharomyces cerevisiae.The Journal of biological chemistry · 2010Article
- Synergistic operation of four cis-acting elements mediate high level DAL5 transcription in Saccharomyces cerevisiae.FEMS yeast research · 2004Article
- Tor1/2 regulation of retrograde gene expression in Saccharomyces cerevisiae derives indirectly as a consequence of alterations in ammonia metabolism.The Journal of biological chemistry · 2003Article
- A transcriptional switch in the expression of yeast tricarboxylic acid cycle genes in response to a reduction or loss of respiratory function.Molecular and cellular biology · 1999Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.