The Yeast Iron Regulon Is Induced upon Cobalt Stress and Crucial for Cobalt Tolerance

Stadler, Jochen A.; Schweyen, Rudolf J.

doi:10.1074/jbc.m203924200

Cited by 78 publications

(85 citation statements)

References 43 publications

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“…In addition, the oxidative stress responsive genes, such as glutathione peroxidase, thioredoxin and glutaredoxin, were also induced (Table 3). Our results correlated well with a previous report on transcriptional response to cobalt (Stadler and Schweyen, 2002). The study also showed that cobalt stress induces the accumulation of iron in the yeast cells.…”

Section: Resultssupporting

confidence: 82%

DNA microarray analysis of genomic responses of yeast Saccharomyces cerevisiae to nickel chloride

et al. 2010

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-In order to investigate nickel toxicity against the yeast Saccharomyces cerevisiae, genomic responses to nickel chloride were examined using yeast DNA microarrays. Microarray analysis revealed that exposure to 25 mM nickel chloride for 2 hr induced changes in gene expression in S. cerevisiae. Nickel chloride increased expression levels in 601 genes and decreased expression levels in 696 genes in S. cerevisiae.

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Section: Resultssupporting

confidence: 82%

DNA microarray analysis of genomic responses of yeast Saccharomyces cerevisiae to nickel chloride

et al. 2010

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“…8A). Deletion of AFT1 also abrogated the Co 2ϩ resistance in wild type and ⌬mrs3⌬mrs4 cells, confirming a recent report that Co 2ϩ resistance was due to the expression of Aft1p-regulated genes (21). Transformation of wild type cells with an AFT1-1 up allele results in increased expression of the CTR1-LacZ reporter construct (Fig.…”

Section: Changes In Copper Metabolismsupporting

confidence: 72%

A Mitochondrial-Vacuolar Signaling Pathway in Yeast That Affects Iron and Copper Metabolism

Kaplan

2004

Journal of Biological Chemistry

102

130

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Mitochondria utilize iron, but the transporters that mediate mitochondrial iron uptake and efflux are largely unknown. Cells with a deletion in the vacuolar iron/manganese transporter Ccc1p are sensitive to high iron. Overexpression of MRS3 or MRS4 suppresses the high iron sensitivity of ⌬ccc1 cells. MRS3 and MRS4 have recently been suggested to encode mitochondrial iron transporters. We demonstrate that deletion of MRS3 and MRS4 severely affects cellular and mitochondrial metal homeostasis, including a reduction in cytosolic and mitochondrial iron acquisition. We show that vacuolar iron transport is increased in ⌬mrs3⌬mrs4 cells, resulting in decreased cytosolic iron and activation of the iron-sensing transcription factor Aft1p. Activation of Aft1p leads to increased expression of the high affinity iron transport system and increased iron uptake. Deletion of CCC1 in ⌬mrs3⌬mrs4 cells restores cellular and mitochondrial iron homeostasis to near normal levels. ⌬mrs3⌬mrs4 cells also show increased resistance to cobalt but decreased resistance to copper and cadmium. These phenotypes are also corrected by deletion of CCC1 in ⌬mrs3⌬mrs4 cells. Decreased copper resistance in ⌬mrs3⌬mrs4 cells results from activation of Aft1p by Ccc1p-mediated iron depletion, as deletion of CCC1 or AFT1 in ⌬mrs3⌬mrs4 cells restores copper resistance. These results suggest that deletion of mitochondrial proteins can alter vacuolar metal homeostasis. The data also indicate that increased expression of the AFT1-regulated gene(s) can disrupt copper homeostasis.Two important aspects of cellular iron metabolism are localized to mitochondria, heme synthesis and iron-sulfur cluster synthesis. Both synthetic pathways require iron import into mitochondria, but little is known about mitochondrial transporters for either import or export of iron. Recent studies have shown that deletion of both MRS3 and MRS4, members of the mitochondrial carrier family, results in decreased mitochondrial iron content. Double deletion strains (⌬mrs3⌬mrs4) demonstrate a low iron growth defect and decreased heme and iron-sulfur cluster synthesis (1, 2). Furthermore, Foury and Roganti (1) deleted MRS3 and MRS4 in a strain lacking Yfh1p, the yeast frataxin homologue. Loss of Yfh1p leads to defects in iron-sulfur cluster synthesis (3-5) and excessive mitochondrial iron accumulation (6). ⌬yfh1 cells are protected from mitochondrial iron toxicity when MRS3 and MRS4 are deleted (1). Deletion of these genes does not completely abrogate mitochondrial iron uptake, leading to the suggestion that they encode mitochondrial iron transporters whose function only becomes apparent under low iron conditions (2).Other characteristics of ⌬mrs3⌬mrs4 cells are inconsistent with a role for these genes simply as mitochondrial iron transporters, as broad effects on transition metal metabolism have been observed. In particular, ⌬mrs3⌬mrs4 cells show increased cellular iron acquisition due to up-regulation of the iron regulon (1, 2). Disruption of the MRS3/MRS4 homologue in Cryptococcus neoforma...

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“…cerevisiae is an ideal eukaryotic organism to study global gene expression in response to a variety of environmental variations including oxidative stress, heavy metal ions and heat shock. Previously, yeast transcriptome analysis under surplus cobalt stress revealed that the iron regulon participates in cobalt tolerance (Stadler and Schweyen, 2002). In contrast, we observed that surplus iron can serve as a growth stimulator to significantly accelerate the growth of yeast cells.…”

Section: Introductionmentioning

confidence: 58%

Expression Profiling Reveals an Unexpected Growth-Stimulating Effect of Surplus Iron on the Yeast Saccharomyces cerevisiae

Wang

2012

Molecules and Cells

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Iron homeostasis plays a crucial role in growth and division of cells in all kingdoms of life. Although yeast iron metabolism has been extensively studied, little is known about the molecular mechanism of response to surplus iron. In this study, expression profiling of Saccharomyces cerevisiae in the presence of surplus iron revealed a dual effect at 1 and 4 h. A cluster of stress-responsive genes was upregulated via activation of the stress-resistance transcription factor Msn4, which indicated the stress effect of surplus iron on yeast metabolism. Genes involved in aerobic metabolism and several anabolic pathways are also upregulated in iron-surplus conditions, which could significantly accelerate yeast growth. This dual effect suggested that surplus iron might participate in a more complex metabolic network, in addition to serving as a stress inducer. These findings contribute to our understanding of the global response of yeast to the fluctuating availability of iron in the environment.

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The Yeast Iron Regulon Is Induced upon Cobalt Stress and Crucial for Cobalt Tolerance

Cited by 78 publications

References 43 publications

DNA microarray analysis of genomic responses of yeast Saccharomyces cerevisiae to nickel chloride

DNA microarray analysis of genomic responses of yeast Saccharomyces cerevisiae to nickel chloride

A Mitochondrial-Vacuolar Signaling Pathway in Yeast That Affects Iron and Copper Metabolism

Expression Profiling Reveals an Unexpected Growth-Stimulating Effect of Surplus Iron on the Yeast Saccharomyces cerevisiae

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