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A Candida auris –specific adhesin, Scf1 , governs surface association, colonization, and virulence
Open accessAbstract
Candida auris is an emerging fungal pathogen responsible for health care–associated outbreaks that arise from persistent surface and skin colonization. We characterized the arsenal of adhesins used by C. auris and discovered an uncharacterized adhesin, Surface Colonization Factor (Scf1), and a conserved adhesin, Iff4109, that are essential for the colonization of inert surfaces and mammalian hosts. SCF1 is apparently specific to C. auris , and its expression mediates adhesion to inert and biological surfaces across isolates from all five clades. Unlike canonical fungal adhesins, which function through hydrophobic interactions, Scf1 relies on exposed cationic residues for surface association. SCF1 is required for C. auris biofilm formation, skin colonization, virulence in systemic infection, and colonization of inserted medical devices.
Overview
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TL;DR
The paper identifies Scf1 (SCF1; B9J08_001458), a *Candida auris*–specific adhesin, and the conserved adhesin IFF4109 as key mediators of surface attachment, colonization, biofilm formation, and virulence. Scf1 promotes adhesion via exposed cationic residues rather than canonical hydrophobic interactions, and its expression varies across *C. auris* isolates in a manner correlated with adhesive capacity.
Key findings
- Of twelve *C. auris* ALS/IFF-HYR adhesin deletion mutants tested, only deletion of IFF4109 (B9J08_004109) caused an adhesive defect; a screen of 2,560 insertional mutants found the greatest adhesion loss in tnSWI1 (B9J08_003460) and tnBCY1 (B9J08_002818), with SCF1 (B9J08_001458) as the strongest dysregulated gene in tnSWI1.
- SCF1 is apparently specific to *C. auris* and *C. haemulonii*. Across 23 *C. auris* isolates from all five clades, adhesion varied significantly (p=2×10⁻¹⁶, F=35.06, one-way ANOVA), whereas 19 diverse *C. albicans* isolates showed no significant adhesive variation (p=0.054, F=1.856). SCF1 transcript abundance correlated with adhesion (r=0.87, p=8.4×10⁻⁸), while IFF4109 did not (r=0.3, p=0.25).
- Scf1-mediated adhesion does not depend on cell surface hydrophobicity: IFF4109 deletion reduced hydrophobicity, but SCF1 deletion or overexpression did not. Only SCF1 mediated adhesion to a hydrophilic, vacuum plasma–treated polystyrene surface. High arginine concentrations ablated AR0382 adhesion, and the HHRR cationic-aromatic cluster at residues 52–55 was required for adhesion; a wild-type Scf1 peptide (residues 50–62) bound polystyrene microspheres, while mutation of HHRR ablated binding.
- SCF1 and IFF4109 were functionally redundant for biofilm formation, but loss of both ablated AR0382 biofilm and rat central venous catheter colonization; SCF1 overexpression potentiated AR0387 colonization. Loss of both adhesins reduced human skin explant and murine skin colonization and reduced dissemination to kidneys and heart. In disseminated infection, wild-type AR0382 caused 100% mortality within 12 days versus 20% mortality after 21 days for the mutant; SCF1 overexpression reduced median survival of AR0387-infected mice from 18.5 days to 11.5 days.
Methods
- Genetic and phenotypic assays in *C. auris* clade I AR0382: individual deletion mutants for twelve ALS/IFF-HYR adhesin genes, a 2,560-member insertional mutant library screen, flow cytometric adhesion assays to polystyrene microspheres, RNA-seq, complementation, epitope tagging, overexpression, AlphaFold2 modeling, peptide binding assays, MATH hydrophobicity assays, and biofilm assays.
- Isolate panel and expression analysis: adhesion measured for 23 *C. auris* isolates representing all five clades and 19 genetically diverse *C. albicans* clinical isolates; SCF1 and IFF4109 transcript abundance compared with adhesion.
- In vivo and ex vivo colonization/infection models: polyethylene rat central venous catheters, ex vivo human skin explants, in vivo murine skin, and immunosuppressed mice infected intravenously with 5×10⁷ *C. auris* cells; histopathology at 7 days and survival monitored for 21 days. Statistical tests included one-way ANOVA with post-hoc tests, Student’s t-test, Pearson correlation, and Mantel-Haenszel log-rank test with Benjamini-Hochberg correction.
Limitations
- Stated in the paper: the mechanisms by which SCF1 and IFF4109 interact with host systems remain unclear; the selective pressure governing differential SCF1 expression is unknown; and whether the lack of surface-association phenotypes for other conserved adhesin genes reflects functional or regulatory divergence remains to be explored.
- Evident from the text: many mechanistic and virulence experiments focus on the clade I AR0382 background and selected comparator isolates, so generalizability across all *C. auris* lineages is not fully established. The paper also relies on in vitro adhesion/biofilm assays and animal or ex vivo models, which may not fully recapitulate human colonization and infection. No dedicated limitations section is present in the provided text.
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64 Own result · 26 Sources not found · 12 Own interpretation · 2 No basis given
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In the paper
“The nonspecific surface association driven by SCF1 does not occur through canonical hydrophobic interactions, but rather through cation-substrate interactions.”
§ association, colonization, and virulence > One-Sentence Summary:
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In the paper
“SCF1 is critical for biofilm formation in vitro, robust colonization of in vivo central venous catheters, colonization of both human and murine skin, and virulence in disseminated infection.”
§ association, colonization, and virulence > One-Sentence Summary:
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Murine and ex vivo human skin models reflect clinically relevant colonization and disseminated infection in humans.
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In the paper
“Complementation with an epitope-tagged SCF1 allele in the endogenous locus rescued the adhesive defect, and the epitope-tagged Scf1 protein localized to the cell surface, consistent with its role as an adhesin (Fig. 1F, Fig. 1G).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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In the paper
“In contrast, a similar analysis of 19 genetically diverse C. albicans clinical isolates showed no significant adhesive variation (p=0.054,F=1.856, one-way ANOVA), indicating the surface association strategies of C. auris are more plastic than C. albicans (Fig. 2C).”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
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In the paper
“C. auris isolates from diverse and similar genetic lineages exhibit striking divergence in terms of substrate association, and this phenotypic plasticity is tightly correlated with strain-specific transcriptional control of SCF1.”
§ association, colonization, and virulence > One-Sentence Summary:
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In the paper
“We found that C. auris does not primarily rely on conserved adhesins for surface attachment.”
§ association, colonization, and virulence > One-Sentence Summary:
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- Rests on an assumption: Adhesion to polymer substrates is a valid model for surface association and colonization.
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In the paper
“Deletion of the B9J08_001458 ORF in AR0382 conferred a substantial adhesive defect, thus we refer to the gene as Surface Colonization Factor (SCF1) (Fig. 1F).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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In the paper
“SCF1 is critical for biofilm formation in vitro, robust colonization of in vivo central venous catheters, colonization of both human and murine skin, and virulence in disseminated infection.”
§ association, colonization, and virulence > One-Sentence Summary:
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Rests on an assumption: Murine and ex vivo human skin models reflect clinically relevant colonization and disseminated infection in humans.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Complementation with an epitope-tagged SCF1 allele in the endogenous locus rescued the adhesive defect, and the epitope-tagged Scf1 protein localized to the cell surface, consistent with its role as an adhesin (Fig. 1F, Fig. 1G).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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“Compared to the AR0382 parent, the tnSWI1 mutant exhibited no significant transcriptional dysregulation of the ALS or IFF/HYR adhesins, suggesting alternative mediators of adhesion (Fig. 1D).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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- Probably not a substantial claim. 18
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“Notably, deletion of IFF4109 in the Δscf1 background did not significantly reduce attachment beyond deletion of SCF1 alone, suggesting non-additive roles for these adhesins (Fig. 1F).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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“Notably, this same gene was also strongly downregulated in the tnBCY1 mutant while IFF4109 was not (Fig. S2).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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In the paper
“SCF1 is encoded in a genomic locus in C. auris and C. haemulonii that is syntenic, lacking an SCF1 homolog, even to distantly related species (Fig. 2A).”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
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“The strongest, most significantly dysregulated gene in tnSWI1 was an uncharacterized ORF (B9J08_001458), which had no significant primary sequence homology to characterized genes (Fig. 1D).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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In the paper
“SCF1 is necessary and sufficient for robust attachment of C. auris cells to polymer substrates.”
§ association, colonization, and virulence > One-Sentence Summary:
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It may state two separate claims as one.
- Rests on an assumption: Adhesion to polymer substrates is a valid model for surface association and colonization.
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In the paper
“Although the C. haemulonii SCF1 homolog functionally complements Δscf1 in C. auris, it is not essential for adhesion in C. haemulonii and shows poor expression across isolates, indicating reliance on SCF1 for adhesion is specific to C. auris (Fig. S4).”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
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In the paper
“Of the twelve adhesin mutants, only deletion of IFF4109 (B9J08_004109) conferred an adhesive defect, while still failing to completely ablate attachment (Fig. 1A).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
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“However, IFF4892 encodes the entire canonical adhesin architecture and shows similar expression to IFF4109, but of the two, only IFF4109 is required for adhesion, suggesting individual adhesins mediate specific adhesive mechanisms (Fig. 1A, Fig. S3B) (25).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
What the sources say
- Not matchedcites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“Such functional specificity is shown by increased flocculation and aggregation associated with overexpression of ALS4112, while these phenotypes are not associated with SCF1, despite its transcriptional expression being among the highest 2.5% of all genes in this strain background (Fig. S3B, Fig. S3C, Fig. S3D) (30,31).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
What the sources say
- Not matchedcites [30]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [31]
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In the paper
“Both IFF4109 and SCF1 mediated adhesion to the hydrophobic substrate (Fig. 3C).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
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In the paper
“Several mutations had no adhesive impact, but an R54A R55A mutant exhibited a modest adhesive defect, while showing no discernable effect on SCF1 transcription, protein expression, or localization (Fig. S10).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
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In the paper
“Similarly, overexpression of SCF1 reduced the median survival of mice infected with AR0387 from 18.5 days to 11.5 days and ablated the difference in overall survival between the less virulent AR0387 and the more virulent AR0382 (Fig. 5G).”
§ association, colonization, and virulence > SCF1 promotes long-term colonization and virulence
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It may state two separate claims as one.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In AR0382 and AR0387, the SCF1 locus is invariant, but other isolates exhibit allelic variation in, primarily concentrated in the low complexity tandem repeats (Table S1).”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
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In the paper
“The two adhesins were functionally redundant, and deletion of both was required to ablate biofilm formation in AR0382, suggesting the partial adhesive contributions of each is sufficient to establish colonization (Fig. S13A).”
§ association, colonization, and virulence > SCF1 promotes long-term colonization and virulence
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In the paper
“However, SCF1 does not exhibit significant primary sequence homology to S. cerevisiae FLO11 and lacks conservation of the canonical aromatic bands responsible for adhesive functions in true FLO11 homologs (Fig. S8A, Fig. S8B) (32,35).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
What the sources say
- Not matchedcites [32]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [35]
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In the paper
“The wild type Scf1 peptide was similarly able to adhere to phosphotidylcholine microparticles, and SCF1 expression potentiated lipid particle binding by C. auris cells, suggesting SCF1 may also contribute to association with biotic substrates (Fig. S12).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
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In the paper
“Importantly, the magnitude of overexpression using the TEF1 promoter (approximately 2 8 -fold increase) was similar to and did not exceed the naturally varying magnitude of expression difference between the two wild type isolates AR0382 and AR0387 (approximately 2 9 -fold change) (Fig. 2D, Fig. 2E).”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
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In the paper
“Loss of SCF1 and IFF4109 substantially attenuated the virulence of AR0382, with the wild type causing 100% mortality within 12 days of infection and the mutant causing 20% mortality after 21 days (Fig. 5G).”
§ association, colonization, and virulence > SCF1 promotes long-term colonization and virulence
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In the paper
“Similar concentrations of NaCl or other non-cationic amino acids did not produce the same effect, while exogenous lysine produced a more modest inhibition of attachment, consistent with lysine's weaker ability to form electrostatic interactions (Fig. 4B) (41).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
What the sources say
- Not matchedcites [41]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The wild-type peptide adhered to polystyrene microspheres, but mutation of the HHRR cluster completely ablated this ability (Fig. 4E, Fig. 4F).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
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In the paper
“Notably, AR0382 and AR0387 still exhibited differential adhesion to the hydrophilic surface, indicating hydrophobic interactions are not primarily responsible for the differential strain phenotypes (Fig. 3D).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
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In the paper
“Deletion of the IFF4109 adhesin in AR0382 reduced cell surface hydrophobicity, which was rescued to wild type levels by complementation (Fig. 3A, Fig. 3B).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
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In the paper
“However, only SCF1 mediated adhesion to the hydrophilic substrate, showing that SCF1 is not dependent on hydrophobicity (Fig. 3D).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Loss of one adhesin did not result in dysregulation of the other, suggesting the interaction is not a regulatory one (Fig. S7).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“SCF1 mediates host colonization and infection phenotypes.”
§ association, colonization, and virulence > Discussion
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In the paper
“IFF4109, but not SCF1, mediates adhesion through cell surface hydrophobicity.”
§ association, colonization, and virulence > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For instance, loss of ALS1 alone reduces Candida albicans adhesion, despite the presence of seven other ALS genes (Fig. S3A) (29).”
§ association, colonization, and virulence > Polymer surface attachment by the adhesin SCF1
What the sources say
- Not matchedcites [29]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“In Candida species, genetic expansion has resulted in the formation of adhesin families containing genes similar in sequence and domain architecture, with adhesive functions that are redundant or specific across family members (23,24).”
§ association, colonization, and virulence > One-Sentence Summary:
What the sources say
- Not matchedcites [23]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“C. auris encodes genes similar to members of the conserved ALS and IFF/HYR adhesin families found across the genus, although these genes may have expanded independently in C. auris and lack clear one-to-one homology with adhesins from well-characterized species.”
§ association, colonization, and virulence > One-Sentence Summary:
What the sources say
- Not matchedcites (24)(25)(26)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“C. auris outbreaks are characterized by persistent colonization of patient skin and abiotic surfaces, which can remain positive for extensive periods and serve as a source of contaminative transmission (8)(9)(10)(11)(12)(13)(14).”
§ association, colonization, and virulence > One-Sentence Summary:
What the sources say
- Not matchedcites (8)(9)(10)(11)(12)(13)(14)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Not matched
In the paper
“For fungal pathogens, attachment is largely mediated by cell surface-exposed adhesin proteins (22).”
§ association, colonization, and virulence > One-Sentence Summary:
What the sources say
- Not matchedcites [22]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Not matched
In the paper
“C. auris also colonizes indwelling medical devices, which act as a risk factor for the development of invasive disease (15)(16)(17)(18)(19)(20)(21).”
§ association, colonization, and virulence > One-Sentence Summary:
What the sources say
- Not matchedcites (15)(16)(17)(18)(19)(20)(21)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“For these organisms, cation-dependent surface interactions promote adhesion in aqueous and highly ionic environments (36-39).”
§ association, colonization, and virulence > Discussion
What the sources say
- Not matchedcites [36]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [37]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [38]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [39]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Mediation of hydrophobic interactions is largely conserved among fungal adhesins, consistent with the adhesive mechanism of the conserved IFF4109 (32)(33)(34).”
§ association, colonization, and virulence > Discussion
What the sources say
- Not matchedcites (32)(33)(34)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Prior work suggests vaccination or monoclonal antibody therapy targeting Als or Iff/Hyr adhesins may offer protection against lethal C. auris infection (27,47).”
§ association, colonization, and virulence > Discussion
What the sources say
- Not matchedcites [27]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [47]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings show that sequence variation between these two SCF1 alleles does not intrinsically contribute to functional differences in adhesion, and that other factors may also influence adhesive capacity.”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Notably, we observed widespread differential regulation of SCF1 among C. auris isolates regardless of clade, suggesting transcriptional control of this adhesin has adapted more recently than clade separation.”
§ association, colonization, and virulence > Discussion
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Interestingly, similar patterns of cation-aromatic clusters are also abundant in some lipid-binding proteins (40,43).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
What the sources say
- Not matchedcites [40]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [43]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Elevated cell surface hydrophobicity likewise promotes affinity for hydrophobic substrates (33).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
What the sources say
- Not matchedcites [33]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Adhesive systems in many marine organisms rely on similarly cation-rich proteins, which act through displacement of hydrated ions at the surface-liquid interface or direct cation-π interactions with substrates (36-40).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
What the sources say
- Not matchedcites [36]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [37]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [38]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [39]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [40]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Not matched
In the paper
“For other Candida species, adhesion to abiotic substrates is often nonspecific, with adhesins promoting affinity for hydrophobic substrates (32)(33)(34).”
§ association, colonization, and virulence > SCF1 and IFF4109 have distinct nonspecific mechanisms
What the sources say
- Not matchedcites (32)(33)(34)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“C. auris encodes genes similar to the conserved ALS and IFF/HYR adhesin families, and proposed models suggest differential utilization of these adhesins may contribute to epidemiological differences among isolates (25, 27).”
§ association, colonization, and virulence > Discussion
What the sources say
- Not matchedcites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [27]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“We measured the importance of these adhesins for biofilm growth, which can promote prolonged environmental persistence (11,(44)(45)(46).”
§ association, colonization, and virulence > SCF1 promotes long-term colonization and virulence
What the sources say
- Not matchedcites (11,(44)(45)(46)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our findings suggest the C. aurisspecific adhesin SCF1 and the conserved adhesin IFF4109 are the principal mediators of association with abiotic surfaces, and additionally contribute substantially to infection and long-term colonization of both biological and abiotic surfaces.”
§ association, colonization, and virulence > Discussion
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Still, differential utilization of SCF1 by different isolates suggests an unknown selective pressure may govern its expression.”
§ association, colonization, and virulence > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“C. auris has been isolated from the coastal wetlands of the Andaman Islands and from a Colombian estuary, suggesting a possible marine natural habitat, and this ecological niche may have conferred similar selective pressures on adhesion mechanisms (48,49).”
§ association, colonization, and virulence > Discussion
What the sources say
- Not matchedcites [48]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [49]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“C. auris has been isolated from the coastal wetlands of the Andaman Islands and from a Colombian estuary, suggesting a possible marine natural habitat, and this ecological niche may have conferred similar selective pressures on adhesion mechanisms (48,49).”
§ association, colonization, and virulence > Discussion
What the sources say
- Not matchedcites [48]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [49]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
The paper relies on this without support.
Colonization requires the initial physical association and attachment between fungal cells and substrate.
“Colonization requires the initial physical association and attachment between fungal cells and substrate.”
The paper relies on this without support.
Adhesion to polymer substrates is a valid model for surface association and colonization.
“we measured the adhesion between fungal cells and polymer substrates as a model for surface association.”
The paper relies on this without support.
Murine and ex vivo human skin models reflect clinically relevant colonization and disseminated infection in humans.
“we also investigated the importance of these adhesins in disseminated infection.”
The paper relies on this without support.
AlphaFold2 structural predictions reflect the actual structure and adhesive behavior of Scf1.
“we examined the apical N-terminal domain using AlphaFold2, which suggested this domain contains a core Fibronectin-type III fold similar to the FLO11 family of adhesins characterized in Saccharomyces cerevisiae and conserved throughout Ascomycota (Fig. S8A) (32,35).”
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 cited source doesn’t support the claim as written.
In the citing paper
“unlike C. albicans, which contains at least 11 Als adhesins, thus far only 3 ALS genes have been identified in C. auris (20, 22).”
From The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [22]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe cited source doesn’t support the claim as written.
In the citing paper
“The cell wall adhesin Als4 plays a central role in biofilm formation in C. auris and is required for adhesion to both biotic and abiotic surfaces11,14,17,50,52.”
From The Wor2 phenotypic switching regulator controls biofilm formation in Candida auris (2026) · cites this paper as [14]
Checked by a reasoning model — may be wrong.
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
“In addition, understanding the skin immune responses against C. auris is critical, as the murine skin model is widely used to study disease pathogenesis and C. auris-host interactions [4, 16–20].”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [17]
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
“C. auris possesses a unique cell wall, adhesin proteins, and colonizing factors to thrive in the skin [13, 17, 36]”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [17]
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 C. auris genome codes for several species-specific cell surface glycoproteins that may facilitate C. auris adhesion to different substrates (20, 22).”
From The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [22]
Experimental — accuracy not yet measured
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
“we tested the adherence capacity of representative C. auris isolates from four clades (Fig. 1a). Consistent with previous reports on plastic adhesion29 and skin adherence21, we observed variation in keratinocyte adherence between these four representative strains (Fig. 1a).”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [29]
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
“C. auris exhibits a striking predilection for colonizing the human skin, enabling nosocomial transmission and outbreaks of fungemia and deep-seated infections [3–7].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“By performing an elegant forward genetic screen of insertional mutants in C. auris, Santana and colleagues identified a novel adhesin, Scf1 (surface colonizing factor), which promotes fungal adhesion to inert abiotic surfaces through cation-dependent interactions and enhances biofilm formation on murine and human skin [6].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“Furthermore, strains belonging to clades I and IV uncoordinatedly express SCF1 and ALS4112, with regulation independent among the individual strains.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“On the other hand, clade II had low expression of SCF1 and ALS4112, and exhibited low adherence capacity.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“suggesting a vital role of these adhesins in C. auris colonization of the skin [6,11].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“Moreover, deletion of Δscf1Δiff4109 and ΔAls4112 significantly reduced skin colonization, suggesting a vital role of these adhesins in C. auris colonization of the skin [6,11].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“C. auris strains belonging to clade III highly express SCF1 and ALS4112, associated with greater adherence capacity.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“Recent studies suggest that the gene expression of SCF1 and ALS4112 varies among different clades and clinical strains of C. auris, and exhibits a strong positive correlation with C. auris adherence activity [6,11].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
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
“Adhesion to inert surface was essentially triggered by Scf1.”
From Ume6-dependent pathways of morphogenesis and biofilm formation in Candida auris (2024) · cites this paper as [27]
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
“C. auris displays at least three Als-like, eight Hyr/Iff-like, and one species-specific adhesin (Scf1) (27, 53–55) (Table S3).”
From Ume6-dependent pathways of morphogenesis and biofilm formation in Candida auris (2024) · cites this paper as [27]
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
“Scf1 is unique to C. auris and has a different adhesion mechanism compared to other adhesins (27).”
From Ume6-dependent pathways of morphogenesis and biofilm formation in Candida auris (2024) · cites this paper as [27]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Candida auris is an emerging multidrug-resistant skin-tropic fungal pathogen that causes serious human infections.”
From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“C. auris is an emerging fungal pathogen that can cause serious human infections [1,5,38,39].”
From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“Both SCF1 and IFF4109 are functionally redundant for biofilm formation (22)”
From The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [22]
The cited source says what the claim attributes to it.
In the citing paper
“a C. auris-specific adhesin, Scf1, and the Iff family member, B9J08_004109 (IFF4109), were recently identified for their roles in surface colonization, adhesion, and virulence (22).”
From The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [22]
The cited source says what the claim attributes to it.
In the citing paper
“The genome of C. auris is reported to contain adhesins belonging to ALS and the IFF/HYR family (20, 22).”
From The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [22]
The cited source says what the claim attributes to it.
In the citing paper
“Our recent study demonstrated the role of two adhesins, Scf1 and Iff4109, in promoting skin colonization and disease29.”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [29]
The cited source says what the claim attributes to it.
In the citing paper
“Notably, IFF4109 has previously been implicated in C. auris systemic infection29.”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [29]
The cited source says what the claim attributes to it.
In the citing paper
“We used whole-genome sequencing and insertion mapping to identify an insertion in the gene B9J08_004112, which encodes an ALS adhesin protein on the cell surface, referred to as Als411229, and in the gene B9J08_003899, which encodes a protein homologous to the Saccharomyces cerevisiae Mub1 protein, a subunit of a ubiquitin ligase complex44.”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [29]
The cited source says what the claim attributes to it.
In the citing paper
“Previously, we reported that two C. auris adhesins, Scf1 and Iff4109, contribute to skin colonization29”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [29]
The cited source says what the claim attributes to it.
In the citing paper
“Unlike other Candida species, C. auris exhibits a distinct capacity for persistent skin colonization.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“SCF1 functions redundantly with the adhesin IFF4109, a member of the IFF/HYR adhesin family, as their double deletion in the Δscf1 Δiff4109 mutant strain significantly decreased skin colonization.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“Notably, SCF1 expression varies between C. auris clades and within strains of the same clade and correlates with adhesive capacity; thus, SCF1 expression is low in the poorly adherent strain AR0387 and elevated in the highly adherent strain AR0382.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, overexpression of SCF1 in the poorly adherent strain AR0387 restored its adherence capacity and increased its colonization potential in murine and human skin [6].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“These data confirm the crucial role of Scf1 in adhesion to inert surfaces as recently described (27, 40).”
From Ume6-dependent pathways of morphogenesis and biofilm formation in Candida auris (2024) · cites this paper as [27]
The cited source says what the claim attributes to it.
In the citing paper
“The crucial role of Scf1 in adhesion and biofilm formation has been recently demonstrated (27, 40).”
From Ume6-dependent pathways of morphogenesis and biofilm formation in Candida auris (2024) · cites this paper as [27]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ association, colonization, and virulence > Discussion
“(D) SCF1 transcript abundance (top panel) but not IFF4109 transcript abundance (bottom panel) is associated with adhesion to polystyrene in the same 23 C. auris isolates from (A).”
§ association, colonization, and virulence > Discussion
“(B) Adhesion of 23 C. auris clinical isolates from all 5 clades.”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ association, colonization, and virulence > Abstract
“SCF1 is apparently specific to C. auris and its expression mediates adhesion to inert and biological surfaces across isolates from all five clades.”
§ association, colonization, and virulence > C. auris relies on SCF1 for adhesive plasticity
“Although the C. haemulonii SCF1 homolog functionally complements Δscf1 in C. auris, it is not essential for adhesion in C. haemulonii”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ association, colonization, and virulence > Abstract
“SCF1 is required for C. auris biofilm formation, skin colonization, virulence in systemic infection, and colonization of inserted medical devices.”
§ association, colonization, and virulence > SCF1 promotes long-term colonization and virulence
“The two adhesins were functionally redundant, and deletion of both was required to ablate biofilm formation in AR0382”
Citations
Cites
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Fiji: an open-source platform for biological-image analysis
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Trimmomatic: a flexible trimmer for Illumina sequence data
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Fast and accurate short read alignment with Burrows-Wheeler transform
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STAR: ultrafast universal RNA-seq aligner
Dobin, A., Davis, C. A., Schlesinger, F., Drenkow, J., Zaleski, C., Jha, S., Batut, P., Chaisson, M., & Gingeras, T. R. (2013) · Bioinformatics · doi:10.1093/bioinformatics/bts635 · Cited by 51,709
Cutadapt removes adapter sequences from high-throughput sequencing reads
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featureCounts: an efficient general purpose program for assigning sequence reads to genomic features
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ColabFold - Making protein folding accessible to all
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Primer-BLAST: A tool to design target-specific primers for polymerase chain reaction
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Cited by
Sorted by citations
Lass‐Flörl, C., Kanj, S. S., Govender, N. P., Thompson, G. R., Ostrosky-Zeichner, L. L., & Govrins, M. A. (2024) · Nature Reviews Disease Primers · doi:10.1038/s41572-024-00503-3 · Cited by 345
Bloodstream infections: mechanisms of pathogenesis and opportunities for intervention
Holmes, C. L., Albin, O. R., Mobley, H. L. T., & Bachman, M. A. (2024) · Nature Reviews Microbiology · doi:10.1038/s41579-024-01105-2 · Cited by 157
Lionakis, M. S., & Chowdhary, A. (2024) · New England Journal of Medicine · doi:10.1056/nejmra2402635 · Cited by 130
Fungal biofilms in human health and disease
Ramage, G., Kean, R., Rautemaa-Richardson, R., Williams, C., & Lopez-Ribot, J. L. (2025) · Nature Reviews Microbiology · doi:10.1038/s41579-025-01147-0 · Cited by 72
Mechanisms of pathogenicity for the emerging fungus Candida auris
Horton, M. V., Holt, A. M., & Nett, J. E. (2023) · PLOS Pathogens · doi:10.1371/journal.ppat.1011843 · Cited by 67
Self-citation
Metadata
- Authors
- Santana, D. J., Anku, J. A. E., Zhao, G., Zarnowski, R., Johnson, C. J., Hautau, H., Visser, N. D., Ibrahim, A. S., Andes, D., Nett, J. E., Singh, S., & O’Meara, T. R.
- Affiliations
- University of Michigan (US)
- University of Ghana (GH)
- Department of Medicine, University of Wisconsin, Madison, WI, USA.
- University of Wisconsin–Madison (US)
- University of California, Los Angeles (US)
- Corresponding author
- O’Meara, Teresa R.
- ORCID
- Venue
- Science
- Published
- 2023-09-29
- Volume
- 381
- Issue
- 6665
- Pages
- 1461-1467
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC11235122
- OpenAlex
- W4387128705
- Semantic Scholar
- e0262fbfb5177b14e3b79fa23998bb062df14f12
- Cited by
- 142
- References
- 76
- Citations by year
- 2026: 65 · 2025: 40 · 2024: 34 · 2023: 3
- FWCI
- 26.50
- Type
- journal article
- Language
- en
- Open access
- green
- escholarship.org
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- PubMed Central (submittedVersion)
- Funders
- American Heart Association (938451)
- National Institutes of Health (5t32ai007413-32, T32 AI00,7413, R21AI159583, R01AI073289, T32AI007528, R01AI145939, KL2TR001882)
- Japan Atomic Energy Agency
- National Institute of Allergy and Infectious Diseases (T32-AI-007413, R01-AI073289, R21 AI159583, T32-AI007528, F31AI169823, R01 AI145939, R01AI141202, R01 AI063503, R21 AI169186)
- National Center for Advancing Translational Sciences (KL2TR001882)
- Clinical and Translational Science Institute, University of California, Los Angeles (KL2TR001882)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Infectious Diseases › Fungal Infections and Studies
- Keywords
- Candida auris, fungal adhesins, surface colonization, biofilm formation, virulence, skin colonization, medical device colonization, cationic residues, fungal adhesion, emerging fungal pathogens
- MeSH terms
- Protein Domains, Candida auris, Animals, Fungal Proteins, Humans, Microfilament Proteins, Virulence, Mice, Hydrophobic and Hydrophilic Interactions, Candidiasis, Invasive
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.
A language model drew the claims from the paper on 2026-10-23, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-23 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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 ›
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