Cited by 157Fungal and yeast genetics researchAntifungal resistance and susceptibilityFungal Infections and Studies

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Candida albicans Hap43 Is a Repressor Induced under Low-Iron Conditions and Is Essential for Iron-Responsive Transcriptional Regulation and Virulence

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Hsu, Po-Chen, Yang, Cheng-Yao, Lan, Chung-Yu·2011·Eukaryotic Cell

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Abstract

Candida albicans is an opportunistic fungal pathogen that exists as normal flora in healthy human bodies but causes life-threatening infections in immunocompromised patients. In addition to innate and adaptive immunities, hosts also resist microbial infections by developing a mechanism of “natural resistance” that maintains a low level of free iron to restrict the growth of invading pathogens. C. albicans must overcome this iron-deprived environment to cause infections. There are three types of iron-responsive transcriptional regulators in fungi; Aft1/Aft2 activators in yeast, GATA-type repressors in many fungi, and HapX/Php4 in Schizosaccharomyces pombe and Aspergillus species. In this study, we characterized the iron-responsive regulator Hap43, which is the C. albicans homolog of HapX/Php4 and is repressed by the GATA-type repressor Sfu1 under iron-sufficient conditions. We provide evidence that Hap43 is essential for the growth of C. albicans under low-iron conditions and for C. albicans virulence in a mouse model of infection. Hap43 was not required for iron acquisition under low-iron conditions. Instead, it was responsible for repression of genes that encode iron-dependent proteins involved in mitochondrial respiration and iron-sulfur cluster assembly. We also demonstrated that Hap43 executes its function by becoming a transcriptional repressor and accumulating in the nucleus in response to iron deprivation. Finally, we found a connection between Hap43 and the global corepressor Tup1 in low-iron-induced flavinogenesis. Taken together, our data suggest a complex interplay among Hap43, Sfu1, and Tup1 to coordinately regulate iron acquisition, iron utilization, and other iron-responsive metabolic activities.

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Authors: Hsu, P.-C., Yang, C.-Y., & Lan, C.-Y.
Affiliations: Institute of Molecular and Cellular Biology, No. 101, Section 2, Kuang Fu Road, Hsinchu 30013, Taiwan, Republic of China
Animal Technology Institute Taiwan (TW)
National Tsing Hua University (TW)
Corresponding author: Lan, Chung-Yu
ORCID: Hsu, Po-Chen
Yang, Cheng-Yao
Lan, Chung-Yu
Venue: Eukaryotic Cell
Publisher: American Society for Microbiology
Published: 2011-02
Volume: 10
Issue: 2
Pages: 207-225
ISSN: 1535-9778 (ISSN-L)
1535-9786
DOI: 10.1128/ec.00158-10
PMC: PMC3067405
OpenAlex: W2146920262
Cited by: 157
References: 94
Citations by year: 2026: 4 · 2025: 11 · 2024: 10 · 2023: 10 · 2022: 8 · 2021: 10 · 2020: 8 · 2019: 9 · 2018: 9 · 2017: 10 · 2016: 10 · 2015: 8 · 2014: 13 · 2013: 14 · 2012: 14
FWCI: 4.82
Type: journal article
Language: en
Open access: diamond
doi.org
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Eukaryotic Cell (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
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 › Infectious Diseases › Fungal Infections and Studies
Keywords: Candida albicans, iron starvation, Tup1, iron acquisition, iron-sulfur cluster assembly, mitochondrial respiration, fungal virulence, natural resistance to infection, transcriptional repressor
MeSH terms: Iron Deficiencies, Amino Acid Sequence, Animals, Candida albicans, Candidiasis, Cell Nucleus, Female, Flavins, Fungal Proteins, Humans, Iron, Kidney, Mice, Inbred BALB C, Molecular Sequence Data, Repressor Proteins, Virulence, Gene Expression Regulation, Fungal, Sequence Alignment, Gene Deletion, Sequence Homology, Amino Acid, Two-Hybrid System Techniques, Cell Proliferation, Mice

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Candida albicans Hap43 Is a Repressor Induced under Low-Iron Conditions and Is Essential for Iron-Responsive Transcriptional Regulation and Virulence

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