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Cited by 249Fungal and yeast genetics researchAntifungal resistance and susceptibilityFungal Infections and Studies

Regulatory networks affected by iron availability in Candida albicans

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Lan, Chung‐Yu, Rodarte, Gabriel, Murillo, Luis A., Jones, Ted, Davis, Ronald W., Dungan, Jan, Newport, George, Agabian, Nina·2004·Molecular Microbiology
DOI 10.1111/j.1365-2958.2004.04214.x
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Abstract

Summary: Iron, an essential element for almost every organism, serves as a regulatory signal for the expression of virulence determinants in many prokaryotic and eukaryotic pathogens. Using a custom Affymetrix GeneChip© representing the entire Candida albicans genome, we examined the changes in genome‐wide gene expression in this opportunistic pathogen as a function of alterations in environmental concentrations of iron. A total of 526 open reading frame (ORF) transcripts are more highly expressed when the levels of available iron are low, while 626 ORF transcripts are more highly expressed in high‐iron conditions. The transcripts dominantly affected by iron concentration range from those associated with cell‐surface properties to others which affect mitochondrial function, iron transport and virulence‐related secreted hydrolases. Moreover gene expression as assayed in DNA microarrays confirms and extends reports of alterations in cell‐surface antigens and drug sensitivity correlated with iron availability. To understand how these genes and pathways might be regulated, we isolated a gene designated SFU1 that encodes a homologue of the Ustilago maydis URBS1, a transcriptional repressor of siderophore uptake/biosynthesis. Comparisons between wild‐type and SFU1‐null mutant strains revealed 139 potential target genes of Sfu1p; many of which are iron‐responsive. Together, these results not only expand our understanding of global iron regulation in C. albicans, but also provide insights into the potential role of iron availability in C. albicans virulence.

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Crossref · 10.1111/j.1365-2958.2004.04214.x

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  • Sfu1 prevents toxicity in iron replete medium through inhibition of Sef1, and indirectly Hap43, thereby repressing genes involved in iron acquisition.

    “This transcription factor prevents toxicity in iron replete medium through inhibition of Sef1, and indirectly Hap43, thereby repressing genes involved in iron acquisition (Lan et al., 2004).”

    From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Lan et al., 2004

    The 'Iron-responsive genes controlled by SFU1' section reports that Sfu1 represses iron-acquisition genes under high-iron conditions, and Table 3 lists SEF1 as more highly expressed in the SFU1-null mutant. Our copy does not establish that Sfu1 prevents iron toxicity, inhibits Sef1 protein activity, or indirectly inhibits Hap43. Page numbers were not available for these passages. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Hap43 represses the GATA family transcription factor Sfu1.

    “In addition to this, Hap43 represses the GATA family transcription factor Sfu1.”

    From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Lan et al., 2004

    The section ‘Regulation of iron-responsive genes by Sfu1p’ identifies Sfu1 as a fungal GATA-type factor. However, the passages on SFU1 regulation and targeted searches for Hap43 do not establish that Hap43 represses Sfu1. (LLM, conf=0.80)

    Experimental — accuracy not yet measured

  • During iron-replete conditions, repression of Sfu1 expression is lifted, leading to inhibition of Sef1 expression and nuclear localization and repression of iron acquisition genes.

    “During conditions of replete iron, repression of Sfu1 expression is lifted. This leads to inhibition of Sef1 expression and nuclear localization, as well as repression of iron acquisition genes (Lan et al., 2004).”

    From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Lan et al., 2004

    In “Iron-responsive genes controlled by SFU1” (page not provided), the paper reports that Sfu1 represses iron-acquisition genes under high-iron conditions and lists SEF1 among genes upregulated after SFU1 deletion. But “Iron homeostasis and iron-containing proteins” reports SFU1 transcripts under both low- and high-iron conditions, not that repression of SFU1 expression is lifted by high iron. The copy does not establish an effect on Sef1 nuclear localization. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • The analysis of the C. albicans genome has not revealed a siderophore synthesis pathway.

    “The analysis of the C. albicans genome has not revealed a siderophore synthesis pathway (Lan et al., 2004).”

    From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Lan et al., 2004

  • Category 2 contained 31 mutants with general growth defects that were independent of iron supplementation.

    “Category 2 contained another 31 mutants with general growth defects that were independent of iron supplementation (Fig. 1b), including deletions of known and iron-associated genes (YFH1, ATM1) conserved in most fungi such as C. albicans (28, 29) and S. cerevisiae (30, 31).”

    From A novel hybrid iron regulation network combines features from pathogenic and nonpathogenic yeasts (2016) · cites this paper as [29]

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Authors
Lan, C., Rodarte, G., Murillo, L. A., Jones, T., Davis, R. W., Dungan, J., Newport, G., & Agabian, N.
Affiliations
  • University of California, San Francisco (US)
  • Stanford University (US)
Corresponding author
Agabian, Nina
ORCID
Venue
Molecular Microbiology
Publisher
Wiley
Published
2004-08-03
Volume
53
Issue
5
Pages
1451-1469
ISSN
  • 0950-382X (ISSN-L)
  • 1365-2958
DOI
10.1111/j.1365-2958.2004.04214.x
OpenAlex
W2150543962
Cited by
249
References
125
Citations by year
2026: 1 · 2025: 5 · 2024: 11 · 2023: 5 · 2022: 7 · 2021: 7 · 2020: 14 · 2019: 9 · 2018: 5 · 2017: 9 · 2016: 12 · 2015: 9 · 2014: 21 · 2013: 16 · 2012: 13
FWCI
4.47
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Molecular Microbiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Burroughs Wellcome Fund
  • National Institutes of Health (5r01ai033317-08, 5r01de012302-03, PO1DE07946)
  • University of California, San Francisco
  • National Human Genome Research Institute (HG00205)
  • National Institute of Allergy and Infectious Diseases (5R01AI33317)
  • National Institute of Dental and Craniofacial Research (DE 12302-02S2, P01DE007946)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
Keywords
Candida albicans, iron availability, iron regulation, gene expression, virulence, siderophore biosynthesis, siderophore uptake, transcriptional repressor, cell surface antigens, drug sensitivity, mitochondrial function, iron transport, hydrolytic enzymes, opportunistic pathogens
MeSH terms
Amino Acid Sequence, Animals, Candida albicans, Fungal Proteins, Iron, Molecular Sequence Data, Gene Expression Regulation, Fungal, Open Reading Frames, Sequence Alignment, Genome, Fungal, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Periplasmic Binding Proteins

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