Approaches to the Study of Rox1 Repression of the Hypoxic Genes in the YeastSaccharomyces cerevisiae

Zitomer, R S; Limbach, M. Paullin; Rodríguez-Torres, Ana-María; Balasubramanian, Bhuvana; Deckert, Jutta; Snow, Peter M.

doi:10.1006/meth.1996.0422

Cited by 32 publications

(21 citation statements)

References 42 publications

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“…In aerobic cells, Rox1 serves to attenuate activation by both of the metal-responsive activators, Aft1 and Zap1, that control FET4 expression. Rox1 functions by recruiting the Ssn6 and Tup1 repressors to promoters where they block activation by positive factors (38). It is interesting to note that in Candida albicans, Tup1 regulates iron uptake genes in response to iron status (48).…”

Section: Discussionmentioning

confidence: 99%

“…Rox1 Repression Attenuates Activation by Aft1 and Zap1-Rox1 represses gene expression by recruiting the Tup1 and Ssn6 general transcription repressors to its target promoters where they block activation by positive factors also bound to these promoters (38). To determine whether Rox1 attenuates Aft1-and Zap1-mediated FET4 expression, we examined FET4-lacZ expression in wild-type and rox1⌬ cells over a range of iron (Fig.…”

Section: Fet4 Transcription Is Regulated Bymentioning

confidence: 99%

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Combinatorial Control of Yeast FET4 Gene Expression by Iron, Zinc, and Oxygen

Waters

Eide

2002

Journal of Biological Chemistry

127

101

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Acquisition of metals such as iron, copper, and zinc by the yeast Saccharomyces cerevisiae is tightly regulated. High affinity uptake systems are induced under metallimiting conditions to maintain an adequate supply of these essential nutrients. Low affinity uptake systems function when their substrates are in greater supply. The FET4 gene encodes a low affinity iron and copper uptake transporter. FET4 expression is regulated by several environmental factors. In this report, we describe the molecular mechanisms underlying this regulation. First, we found that FET4 expression is induced in iron-limited cells by the Aft1 iron-responsive transcriptional activator. Second, FET4 is regulated by zinc status via the Zap1 transcription factor. We present evidence that FET4 is a physiologically relevant zinc transporter and this provides a rationale for its regulation by Zap1. Finally, FET4 expression is regulated in response to oxygen by the Rox1 repressor. Rox1 attenuates activation by Aft1 and Zap1 in aerobic cells. Derepression of FET4 may allow the Fet4 transporter to play an even greater role in metal acquisition under anaerobic conditions. Thus, Fet4 is a multisubstrate metal ion transporter under combinatorial control by iron, zinc, and oxygen.

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Section: Discussionmentioning

confidence: 99%

Section: Fet4 Transcription Is Regulated Bymentioning

confidence: 99%

Combinatorial Control of Yeast FET4 Gene Expression by Iron, Zinc, and Oxygen

Waters

Eide

2002

Journal of Biological Chemistry

127

101

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“…We also constructed strains that are deleted for YHB1 alone or in combination with COX5a or COX5b. Strains JM43 and DR11 carry functional copies of COX5a and COX5b but should express mainly COX5a when grown under normoxic conditions because COX5b expression is repressed by the Rox1p/Reo1p repressor in the presence of air (38)(39)(40). DR11 is identical to JM43 except that it carries a null mutation in YHB1 (41).…”

Section: Characterization Of Strains Lacking Yhb Va and Vb Singly Omentioning

confidence: 99%

Oxygen-regulated isoforms of cytochrome c oxidase have differential effects on its nitric oxide production and on hypoxic signaling

Castello

Woo

Ball

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

103

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Recently, it has been reported that mitochondria possess a novel pathway for nitric oxide (NO) synthesis. This pathway is induced when cells experience hypoxia, is nitrite (NO 2 ؊ )-dependent, is independent of NO synthases, and is catalyzed by cytochrome c oxidase (Cco). It has been proposed that this mitochondrially produced NO is a component of hypoxic signaling and the induction of nuclear hypoxic genes. In this study, we examine the NO 2 ؊ -dependent NO production in yeast engineered to contain alternative isoforms, Va or Vb, of Cco subunit V. Previous studies have shown that these isoforms have differential effects on oxygen reduction by Cco, and that their genes (COX5a and COX5b, respectively) are inversely regulated by oxygen. Here, we find that the Vb isozyme has a higher turnover rate for NO production than the Va isozyme and that the Vb isozyme produces NO at much higher oxygen concentrations than the Va isozyme. We have also found that the hypoxic genes CYC7 and OLE1 are induced to higher levels in a strain carrying the Vb isozyme than in a strain carrying the Va isozyme. Together, these results demonstrate that the subunit V isoforms have differential effects on NO 2 ؊ -dependent NO production by Cco and provide further support for a role of Cco in hypoxic signaling. These findings also suggest a positive feedback mechanism in which mitochondrially produced NO induces expression of COX5b, whose protein product then functions to enhance the ability of Cco to produce NO in hypoxic/anoxic cells.hypoxia ͉ mitochondria ͉ reactive oxygen species ͉ nitrite ͉ yeast I t has been known for quite some time that the mitochondrial respiratory chain is capable of generating reactive oxygen species (ROS) that account for much of the oxidative stress experienced by cells (1-3). The levels of these ROS increase when electron flow through the respiratory chain is inhibited by respiratory inhibitors (4-6) or altered by uncoupling electron transport from oxidative phosphorylation (7,8). Several studies have shown that exposure of cells and tissues to hypoxia increases ROS levels and oxidative stress (9-11). This increase in oxidative stress during exposure to hypoxia depends on a functional mitochondrial respiratory chain (10). It is currently unclear whether this increase is the result of increased generation or decreased destruction of ROS under hypoxic conditions. In yeast cells, the increase in ROS levels and oxidative stress is transient, as determined by shifting cells from normoxia to anoxia (10). During this shift, cells experience a continuum of decreasing oxygen concentrations and a transient increase in the levels of carbonylation of both mitochondrial and cytosolic protein, an increase in 8-OH-dG levels in mtDNA, and an increase in expression of the SOD1 gene. Many of the proteins that are carbonylated during a shift from normoxia to anoxia are the same proteins that are carbonylated when cells are exposed to menadione, a redox recycling agent that produces elevated intracellular levels of superoxide (12). ...

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“…Tup1, Ssn6) whose complex may modulate the affinity of Rox1 for its binding site on target genes. 215 In addition, promoter searches have shown that nearly one-third of the anaerobically induced genes contain a consensus binding site for the Ucp2 transcription factor. 105 …”

Section: Role Of Haem Concentration In Oxygen Sensingmentioning

confidence: 99%

Role of the non‐respiratory pathways in the utilization of molecular oxygen by Saccharomyces cerevisiae

Rosenfeld

Beauvoit

2003

Yeast

132

110

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Saccharomyces cerevisiae is a facultative anaerobe devoid of mitochondrial alternative oxidase. In this yeast, the structure and biogenesis of the respiratory chain, on the one hand, and the functional interactions of oxidative phosphorylation with the cellular energetic metabolism, on the other, are well documented. However, to our knowledge, the molecular aspects and the physiological roles of the non-respiratory pathways that utilize molecular oxygen have not yet been reviewed. In this paper, we review the various non-respiratory pathways in a global context of utilization of molecular oxygen in S. cerevisiae. The roles of these pathways are examined as a function of environmental conditions, using either physiological, biochemical or molecular data. Special attention is paid to the characterization of the so-called 'cyanide-resistant respiration' that is induced by respiratory deficiency, catabolic repression and oxygen limitation during growth. Finally, several aspects of oxygen sensing are discussed.

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Approaches to the Study of Rox1 Repression of the Hypoxic Genes in the YeastSaccharomyces cerevisiae

Cited by 32 publications

References 42 publications

Combinatorial Control of Yeast FET4 Gene Expression by Iron, Zinc, and Oxygen

Combinatorial Control of Yeast FET4 Gene Expression by Iron, Zinc, and Oxygen

Oxygen-regulated isoforms of cytochrome c oxidase have differential effects on its nitric oxide production and on hypoxic signaling

Role of the non‐respiratory pathways in the utilization of molecular oxygen by Saccharomyces cerevisiae

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