Altered Expression of Selectable Marker URA3 in Gene-Disrupted Candida albicans Strains Complicates Interpretation of Virulence Studies
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The ura-blaster technique for the disruption of Candida albicans genes has been employed in a number of studies to identify possible genes encoding virulence factors of this fungal pathogen. In this study, the URA3-encoded orotidine 5'-monophosphate (OMP) decarboxylase enzyme activities of C. albicans strains with ura-blaster-mediated genetic disruptions were measured. All strains harboring genetic lesions via the ura-blaster construct showed reduced OMP decarboxylase activities compared to that of the wild type when assayed. The activity levels in different gene disruptions varied, suggesting a positional effect on the level of gene expression. Because the URA3 gene of C. albicans has previously been identified as a virulence factor for this microorganism, our results suggest that decreased virulence observed in strains constructed with the ura-blaster cassette cannot accurately be attributed, in all cases, to the targeted genetic disruption. Although revised methods for validating a URA3-disrupted gene as a target for antifungal drug development could be devised, it is clearly desirable to replace URA3 with a different selectable marker that does not influence virulence.
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Loss of HIS3, LEU2, TRP1 or a combination of all three in Candida glabrata does not impact its virulence, unlike deletion of the URA3 marker in Candida albicans which is known to affect its virulence.
“Pertinently, Jacobsen et al. have shown that loss of HIS3, LEU2, TRP1 or a combination of all three in C. glabrata does not impact its virulence, unlike deletion of the URA3 marker in C. albicans which is known to affect its virulence (Lay et al. 1998; Brand et al. 2004; Jacobsen et al. 2010).”
From <i>Candida glabrata</i> : new tools and technologies—expanding the toolkit (2015) · cites this paper as Lay et al. 1998
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References 34 · Cited by 174
- Authors
- Lay, J., Henry, L. K., Clifford, J., Koltin, Y., Bulawa, C. E., & Becker, J. M.
- Affiliations
- University of Tennessee at Knoxville (US)
- Takeda Oncology (United States) (US)
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 1998-11
- Volume
- 66
- Issue
- 11
- Pages
- 5301-5306
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC108662
- OpenAlex
- W2169043974
- Cited by
- 174
- References
- 34
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 3 · 2021: 3 · 2020: 2 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 3 · 2015: 6 · 2014: 16 · 2013: 11 · 2012: 2
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Infection and Immunity (publishedVersion)
- PubMed Central (publishedVersion)
- Europe PMC (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 › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida albicans, URA3, gene disruption, orotidine 5'-monophosphate decarboxylase, virulence factors, selectable marker, gene expression, antifungal drug targets, position effect
- MeSH terms
- Animals, Candida albicans, Enzyme Activation, Fungal Proteins, Orotidine-5'-Phosphate Decarboxylase, Virulence, Gene Expression Regulation, Fungal, Mutagenesis, Insertional, Gene Deletion, Gene Dosage, Mice
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