The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Systematic screens of a Candida albicans homozygous deletion library decouple morphogenetic switching and pathogenicity
Open accessAbstract
Candida albicans is the most common cause of serious fungal disease in humans. Creation of isogenic null mutants of this diploid organism, which requires sequential gene targeting, allows dissection of virulence mechanisms. Published analyses of such mutants show a near-perfect correlation between C. albicans pathogenicity and the ability to undergo a yeast-to-hypha morphological switch in vitro. However, most studies have used mutants constructed with a marker that is itself a virulence determinant and therefore complicates their interpretation. Using alternative markers, we created approximately 3,000 homozygous deletion strains affecting 674 genes, or roughly 11% of the C. albicans genome. Screening for infectivity in a mouse model and for morphological switching and cell proliferation in vitro, we identified 115 infectivity-attenuated mutants, of which nearly half demonstrated normal morphological switching and proliferation. Analysis of such mutants revealed that virulence requires the glycolipid glucosylceramide. To our knowledge, this is the first C. albicans small molecule that has been found to be required specifically for virulence.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“It has been reported that among 674 C. albicans gene-deleted mutants, 59% of these growth-defective mutants were competent for virulence, and 79% of virulence-defective mutants showed a normal growth in vitro, indicating that growth defects were not necessarily correlated to virulence31.”
From The δ subunit of F1Fo-ATP synthase is required for pathogenicity of Candida albicans (2021) · cites this paper as [31]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The growth ability30–32 and virulence factor production31 of C. albicans in the host determine the infection trend, and the former affects the latter to some extent, but the latter is not always affected by the former31.”
From The δ subunit of F1Fo-ATP synthase is required for pathogenicity of Candida albicans (2021) · cites this paper as [31]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“It has been reported that among 674 C. albicans gene-deleted mutants, 59% of these growth-defective mutants were competent for virulence, and 79% of virulence-defective mutants showed a normal growth in vitro, indicating that growth defects were not necessarily correlated to virulence31.”
From The δ subunit of F1Fo-ATP synthase is required for pathogenicity of Candida albicans (2021) · cites this paper as [31]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Importantly, of these complex proteins, orf19.287 and orf19.6607 are fungus specific, and both deleted mutants are attenuated or avirulent (24).”
From Azole Susceptibility and Transcriptome Profiling in Candida albicans Mitochondrial Electron Transport Chain Complex I Mutants (2013) · cites this paper as [24]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Importantly, of these complex proteins, orf19.287 and orf19.6607 are fungus specific, and both deleted mutants are attenuated or avirulent (24).”
From Azole Susceptibility and Transcriptome Profiling in Candida albicans Mitochondrial Electron Transport Chain Complex I Mutants (2013) · cites this paper as [24]
Experimental — accuracy not yet measured
In the citing paper
“This is consistent with the observations of Noble and co-workers that in vitro fitness is not always a reflection of virulence (Noble et al., 2010).”
From The evolution of drug resistance in clinical isolates of Candida albicans. (2015) · cites this paper as Noble et al., 2010
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Nosocomial Bloodstream Infections in United States Hospitals: A Three‐Year Analysis
Edmond, M. B., Wallace, S. E., McClish, D. K., Pfaller, M. A., Jones, R. N., & Wenzel, R. P. (1999) · Clinical Infectious Diseases · doi:10.1086/520192 · Cited by 1,387
Quorum Sensing in the Dimorphic Fungus Candida albicans Is Mediated by Farnesol
Hornby, J. M., Jensen, E. C., Lisec, A. D., Tasto, J. J., Jahnke, B., Shoemaker, R., Dussault, P., & Nickerson, K. W. (2001) · Applied and Environmental Microbiology · doi:10.1128/aem.67.7.2982-2992.2001 · Cited by 983
The distinct morphogenic states of Candida albicans
Sudbery, P., Gow, N., & Berman, J. (2004) · Trends in Microbiology · doi:10.1016/j.tim.2004.05.008 · Cited by 876
The diploid genome sequence of Candida albicans
Jones, T., Federspiel, N. A., Chibana, H., Dungan, J. M., Kalman, S., Magee, B. B., Newport, G., Thorstenson, Y. R., Agabian, N. M., Magee, P. T., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0401648101 · Cited by 784
Zaoutis, T. E., Argon, J., Chu, J., Berlin, J. A., Walsh, T. J., & Feudtner, C. (2005) · Clinical Infectious Diseases · doi:10.1086/496922 · Cited by 784
Noble, S. M., & Johnson, A. D. (2005) · Eukaryotic Cell · doi:10.1128/ec.4.2.298-309.2005 · Cited by 592
Self-citationRecombination-mediated PCR-directed plasmid construction in vivo in yeast
Oldenburg, K. R. (1997) · Nucleic Acids Research · doi:10.1093/nar/25.2.451 · Cited by 516
Roemer, T., Jiang, B., Davison, J., Ketela, T. W., Veillette, K., Breton, A., Tandia, F., Linteau, A., Sillaots, S., Marta, C., et al. (2003) · Molecular Microbiology · doi:10.1046/j.1365-2958.2003.03697.x · Cited by 513
Morphogenesis in Candida albicans
Whiteway, M. S., & Bachewich, C. (2007) · Annual Review of Microbiology · doi:10.1146/annurev.micro.61.080706.093341 · Cited by 408
Rocha, C. R. C., Schröppel, K., Harcus, D., Marcil, A., Dignard, D., Taylor, B. N., Thomas, D. Y., Whiteway, M. S., & Leberer, E. (2001) · Molecular Biology of the Cell · doi:10.1091/mbc.12.11.3631 · Cited by 349
Research works printed but not linked: 1
- Ausubel, F.M. et al. (eds.) Current Protocols in Molecular Biology (John Wiley & Sons, New York, 1990).
Cited by
Sorted by citations
Growth of Candida albicans hyphae
Sudbery, P. E. (2011) · Nature Reviews Microbiology · doi:10.1038/nrmicro2636 · Cited by 1,110
Antifungal Drug Resistance: Molecular Mechanisms in Candida albicans and Beyond
Lee, Y., Puumala, E., Robbins, N., & Cowen, L. E. (2021) · Chemical Reviews · doi:10.1021/acs.chemrev.0c00199 · Cited by 801
Phenotypic Landscape of a Bacterial Cell
Nichols, R. J., Sen, Ś., Choo, Y. J., Beltrão, P., Zietek, M., Chaba, R., Lee, S., Kazmierczak, K. M., Lee, K. J., Wong, A., et al. (2010) · Cell · doi:10.1016/j.cell.2010.11.052 · Cited by 723
A Recently Evolved Transcriptional Network Controls Biofilm Development in Candida albicans
Nobile, C. J., Fox, E. P., Nett, J. E., Sorrells, T. R., Mitrovich, Q. M., Hernday, A. D., Tuch, B. B., Andes, D. R., & Johnson, A. D. (2012) · Cell · doi:10.1016/j.cell.2011.10.048 · Cited by 711
Self-citationRegulatory circuitry governing fungal development, drug resistance, and disease.
Shapiro, R. S., Robbins, N., & Cowen, L. E. (2011) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00045-10 · Cited by 576
Metadata
- Authors
- Noble, S. M., French, S., Kohn, L. A., Chen, V., & Johnson, A. D.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Noble, Suzanne M
- Venue
- Nature Genetics
- Published
- 2010-06-13
- Volume
- 42
- Issue
- 7
- Pages
- 590-598
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC2893244
- OpenAlex
- W2139307267
- Cited by
- 678
- References
- 50
- Citations by year
- 2026: 14 · 2025: 28 · 2024: 31 · 2023: 31 · 2022: 35 · 2021: 53 · 2020: 46 · 2019: 51 · 2018: 45 · 2017: 51 · 2016: 51 · 2015: 50 · 2014: 42 · 2013: 51 · 2012: 45
- FWCI
- 19.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- U.S. Public Health Service (R01 A149187)
- National Institute of Allergy and Infectious Diseases (K08AI062800)
- 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, virulence, infectivity, mouse infection model, glucosylceramide, glycolipids, cell proliferation, fungal pathogenicity
- MeSH terms
- Animals, Candida albicans, Candidiasis, Female, Fungal Proteins, Glucosylceramides, Homozygote, Humans, Mice, Inbred BALB C, Morphogenesis, Mutation, Virulence, Molecular Structure, Gene Library, Survival Analysis, Gene Deletion, Hyphae, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
