Control of Filament Formation in
            <i>Candida albicans</i>
            by the Transcriptional Repressor TUP1

Braun, Burkhard R.; Johnson, Alexander D.

doi:10.1126/science.277.5322.105

Cited by 499 publications

(487 citation statements)

References 27 publications

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“…Transformation of C. albicans was achieved by the lithium acetate method (Braun & Johnson, 1997). Plasmid DNA was isolated and purified from E. coli by alkaline lysis (IshHorowicz & Burke, 1981) and transformation of E. coli was performed using the calcium chloride method (Mandel & Higa, 1970).…”

Section: Methodsmentioning

confidence: 99%

The CaCTR1 gene is required for high-affinity iron uptake and is transcriptionally controlled by a copper-sensing transactivator encoded by CaMAC1

Marvin

Cashmore

2004

Microbiology

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The ability of Candida albicans to acquire iron from the hostile environment of the host is known to be necessary for virulence and appears to be achieved using a similar system to that described for Saccharomyces cerevisiae. In S. cerevisiae, high-affinity iron uptake is dependent upon the acquisition of copper. The authors have previously identified a C. albicans gene (CaCTR1) that encodes a copper transporter. Deletion of this gene results in a mutant strain that grows predominantly as pseudohyphae and displays aberrant morphology in low-copper conditions. This paper demonstrates that invasive growth by C. albicans is induced by low-copper conditions and that this is augmented in a Cactr1-null strain. It also shows that deletion of CaCTR1 results in defective iron uptake. In S. cerevisiae, genes that facilitate high-affinity copper uptake are controlled by a copper-sensing transactivator, ScMac1p. The authors have now identified a C. albicans gene (CaMAC1) that encodes a copper-sensing transactivator. A Camac1-null mutant displays phenotypes similar to those of a Cactr1-null mutant and has no detectable CaCTR1 transcripts in low-copper conditions. It is proposed that high-affinity copper uptake by C. albicans is necessary for reductive iron uptake and is transcriptionally controlled by CaMac1p in a similar manner to that in S. cerevisiae.

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Section: Methodsmentioning

confidence: 99%

The CaCTR1 gene is required for high-affinity iron uptake and is transcriptionally controlled by a copper-sensing transactivator encoded by CaMAC1

Marvin

Cashmore

2004

Microbiology

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“…Less attention has been paid to factors that regulate the hyphal-to-yeast transition, such as the hyphal repressors Nrg1 or Tup1 [31][32][33], or to factors that are important for maintenance or extension of hyphal growth, for example Cln1, Pes1, Eed1 or Ume6 [34][35][36][37][38]. These factors not only govern morphology, but also regulate morphologyassociated genes, for example, HWP1, SOD5, SAP4-6 or ALS3, the expression of which is linked to hyphal growth under most conditions.…”

Section: Proposed Roles Of Yeast and Hyphal Morphologies Of C Albicansmentioning

confidence: 99%

Candida albicansdimorphism as a therapeutic target

Jacobsen

Wilson

Wachtler

et al. 2012

Expert Review of Anti-infective Therapy

321

247

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“…In infected tissue, C. albicans proliferates in both yeast and filamentous forms. The filamentous morphology is repressed by the TUP1 regulator (Braun & Johnson, 1997) and may play a role in invasiveness. Virulence of many pathogens requires expression of specific iron uptake systems, perhaps to counter ironwithholding host defences that operate in different environmental niches (Ratledge & Dover, 2000).…”

Section: Introductionmentioning

confidence: 99%

Reductive iron uptake by Candida albicans: role of copper, iron and the TUP1 regulator

et al. 2002

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High-affinity iron uptake by a ferrous permease in the opportunistic pathogen Candida albicans is required for virulence. Here this iron uptake system has been characterized by investigating three distinct activities : an externally directed surface ferric reductase, a membrane-associated PPD ( pphenylenediamine) oxidase and a cellular ferrous iron transport activity. Copper was required for the PPD oxidase and ferrous transport activities. In contrast, copper was not required for iron uptake from siderophores. Addition of iron to the growth medium repressed ferric reductase and ferrous transport, indicating homeostatic regulation. To identify the genes involved, orthologous mutants of Saccharomyces cerevisiae were transformed with a genomic library of C. albicans. CFL95, a gene with sequence similarity to ferric reductases, restored reductase activity to the orthologous S. cerevisiae mutant. CaFTR2 and CaFTR1, genes with homology to ferrous permeases, conferred ferrous transport activity to the orthologous S. cerevisiae mutant. However, neither a genomic library nor CaFET99, a multicopper oxidase homologue and candidate gene for the PPD oxidase, complemented the S. cerevisiae mutant, possibly because of problems with targeting or assembly. Transcripts for CFL95, CaFTR1 and CaFET99 were strongly repressed by iron, whereas the CaFTR2 transcript was induced by iron. Deletion of the TUP1 regulator perturbed the homeostatic control of reductive iron uptake. Incidentally, iron starvation was noted to induce flavin production and this was misregulated in the absence of TUP1 control. The opposite regulation of two iron permease genes and the role of TUP1 indicate that the process of iron acquisition by C. albicans may be more complex and potentially more adaptable than by S. cerevisiae.

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Control of Filament Formation in Candida albicans by the Transcriptional Repressor TUP1

Cited by 499 publications

References 27 publications

The CaCTR1 gene is required for high-affinity iron uptake and is transcriptionally controlled by a copper-sensing transactivator encoded by CaMAC1

The CaCTR1 gene is required for high-affinity iron uptake and is transcriptionally controlled by a copper-sensing transactivator encoded by CaMAC1

Candida albicansdimorphism as a therapeutic target

Reductive iron uptake by Candida albicans: role of copper, iron and the TUP1 regulator

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