Systematic screens of a Candida albicans homozygous deletion library decouple morphogenetic switching and pathogenicity

Noble, Suzanne M; French, Sarah; Kohn, Lisa A; Chen, Victoria; Johnson, Alexander D

doi:10.1038/ng.605

Cited by 679Fungal and yeast genetics researchAntifungal resistance and susceptibilityFungal Infections and Studies

Systematic screens of a Candida albicans homozygous deletion library decouple morphogenetic switching and pathogenicity

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Noble, Suzanne M, French, Sarah, Kohn, Lisa A, Chen, Victoria, Johnson, Alexander D·2010·Nature Genetics

DOI 10.1038/ng.605PMC PMC2893244

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Abstract

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.

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Growth defects were not necessarily correlated to virulence in C. albicans.
“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]
The Results section, “Quantitative proliferation screen identifies mutants with slow growth phenotypes” (page unavailable), supports the conclusion that poor in vitro growth does not necessarily correlate with reduced virulence. However, it reports 62% of proliferation-defective mutants as competent for infectivity and 77% of infectivity-defective mutants as growing normally in vitro, not the cited 59% and 79%. (LLM, conf=0.90)
Experimental — accuracy not yet measured
Growth ability and virulence factor production of C. albicans in the host determine the infection trend, and growth ability affects virulence factor production to some extent, but virulence factor production is not always affected by growth ability.
“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]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
Among 674 C. albicans gene-deleted mutants, 59% of growth-defective mutants were competent for virulence, and 79% of virulence-defective mutants showed normal growth in vitro.
“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]
The Introduction reports deletions of 674 genes, and the Results section on proliferation supports the conclusion that poor growth in vitro does not necessarily correlate with reduced infectivity. But it reports 42 of 68 (62%) proliferation-defective mutants as competent for infectivity and 89 of 115 (77%) infectivity-defective mutants as growing normally in vitro—not 59% and 79%. (LLM, conf=0.93)
Experimental — accuracy not yet measured
orf19.287 and orf19.6607 are fungus specific.
“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]
The Results section on library construction describes selecting some genes without yeast homologs, but does not identify orf19.287 or orf19.6607 as fungus-specific. Searches for both gene identifiers returned no matching passage in our copy; the virulence Results discuss other named mutants, not these two. (LLM, conf=0.76)
Experimental — accuracy not yet measured
The orf19.287 and orf19.6607 deleted mutants are attenuated or avirulent.
“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]
The Results sections report infectivity defects in the deletion library and virulence defects for other named mutants, but do not identify orf19.287 or orf19.6607 as attenuated or avirulent. Searches for both ORF identifiers and for fungus-specific deletion mutants found no passage addressing these two mutants; the findings for other mutants cannot establish their phenotypes. (LLM, conf=0.72)
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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
ORCID: Noble, Suzanne M
Kohn, Lisa A
Chen, Victoria
Johnson, Alexander D
Venue: Nature Genetics
Publisher: Springer Science and Business Media LLC
Published: 2010-06-13
Volume: 42
Issue: 7
Pages: 590-598
ISSN: 1061-4036 (ISSN-L)
1546-1718
DOI: 10.1038/ng.605
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 › Epidemiology › 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

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Systematic screens of a Candida albicans homozygous deletion library decouple morphogenetic switching and pathogenicity

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