A Mutation in a Purported Regulatory Gene Affects Control of Sterol Uptake in Saccharomyces cerevisiae

Crowley, James H.; Leak, Frank W.; Shianna, Kevin V.; Tove, Shirley; Parks, Leo W.

doi:10.1128/jb.180.16.4177-4183.1998

Cited by 123Fungal and yeast genetics researchLipid metabolism and biosynthesisCancer, Lipids, and Metabolism

A Mutation in a Purported Regulatory Gene Affects Control of Sterol Uptake in Saccharomyces cerevisiae

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Crowley, James H., Leak, Frank W., Shianna, Kevin V., Tove, Shirley, Parks, Leo W.·1998·Journal of Bacteriology

DOI 10.1128/jb.180.16.4177-4183.1998PMC PMC107415

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Abstract

Aerobically growing wild-type strains of Saccharomyces cerevisiae are unable to take exogenously supplied sterols from media. This aerobic sterol exclusion is vitiated under anaerobic conditions, in heme-deficient strains, and under some conditions of impaired sterol synthesis. Mutants which can take up sterols aerobically in heme-competent cells have been selected. One of these mutations, designated upc2-1, gives a pleiotropic phenotype in characteristics as diverse as aerobic accumulation of sterols, total lipid storage, sensitivity to metabolic inhibitors, response to altered sterol structures, and cation requirements. During experiments designed to ascertain the effects of various cations on yeast with sterol alterations, it was observed that upc2-1 was hypersensitive to Ca2+. Using resistance to Ca2+ as a screening vehicle, we cloned UPC2 and showed that it is YDR213W, an open reading frame on chromosome IV. This belongs to a fungal regulatory family containing the Zn(II)2Cys6 binuclear cluster DNA binding domain. The single guanine-to-adenine transition in upc2-1 gives a predicted amino acid change from glycine to aspartic acid. The regulatory defect explains the semidominance and pleiotropic effects of upc2-1.

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ERG11 is transcriptionally regulated by the zinc cluster transcription factor Upc2.
“ERG11 is transcriptionally regulated by the zinc cluster transcription factor Upc2.”
From Gain-of-Function Mutations in UPC2 Are a Frequent Cause of ERG11 Upregulation in Azole-Resistant Clinical Isolates of Candida albicans (2012) · cites this paper as [4]
The Abstract identifies UPC2 as a gene encoding a protein with a Zn(II)2Cys6 DNA-binding motif, and the Discussion describes it as a predicted member of that regulatory protein family. Neither passage establishes that Upc2 transcriptionally regulates ERG11; a search for ERG11 found no passage addressing that relationship. (LLM, conf=0.87)
Experimental — accuracy not yet measured
The upc2-1 mutation is a change of glycine to aspartate at position G888D in the carboxy-terminus of ScUpc2.
“The relevant mutation (upc2-1) [19] is a change of a glycine to an aspartate residue located at position (G888D) in the carboxy-terminus of ScUpc2.”
From The Candida glabrata Upc2A transcription factor is a global regulator of antifungal drug resistance pathways (2021) · cites this paper as [19]
The S. cerevisiae UPC2-1 allele, from which G898D UPC2A was derived, was originally isolated on the basis of permitting aerobic sterol uptake.
“The S. cerevisiae UPC2-1 allele, from which we derived the G898D UPC2A, was originally isolated on the basis of permitting aerobic sterol uptake [19].”
From The Candida glabrata Upc2A transcription factor is a global regulator of antifungal drug resistance pathways (2021) · cites this paper as [19]

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Authors: Crowley, J. H., Leak, F. W., Shianna, K. V., Tove, S., & Parks, L. W.
Affiliations: North Carolina State University (US)
Venue: Journal of Bacteriology
Publisher: American Society for Microbiology
Published: 1998-08-15
Volume: 180
Issue: 16
Pages: 4177-4183
ISSN: 0021-9193 (ISSN-L)
1098-5530
DOI: 10.1128/jb.180.16.4177-4183.1998
PMC: PMC107415
OpenAlex: W2159654630
Cited by: 123
References: 26
Citations by year: 2026: 3 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 3 · 2018: 4 · 2017: 5 · 2015: 3 · 2014: 4 · 2013: 10 · 2012: 2
FWCI: 1.17
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Journal of Bacteriology (publishedVersion)
PubMed Central (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs (TPP 97-003)
Agricultural Research Service
Army Research Office
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords: sterol uptake, UPC2, Saccharomyces cerevisiae, heme deficiency, sterol biosynthesis, pleiotropic mutations, calcium sensitivity, fat deposition, semi-dominant mutation
MeSH terms: Amino Acid Sequence, Base Sequence, Calcium, Fungal Proteins, Genes, Fungal, Genes, Regulator, Genetic Complementation Test, Molecular Sequence Data, Mutation, Saccharomyces cerevisiae, Sterols, Trans-Activators, Open Reading Frames, Saccharomyces cerevisiae Proteins

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A Mutation in a Purported Regulatory Gene Affects Control of Sterol Uptake in Saccharomyces cerevisiae

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