ArticlePLoS genetics2019
Exposure of Candida albicans β (1,3)-glucan is promoted by activation of the Cek1 pathway.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
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- Cinnamaldehyde triggers cell wall remodeling and enhances macrophage-mediated phagocytic clearance ofFrontiers in cellular and infection microbiology · 2025Article
- Glycogen synthase activity inmSphere · 2024Article
- Innate immune signal transduction pathways to fungal infection: Components and regulation.Cell insight · 2024Review
- Impact of secreted glucanases upon the cell surface and fitness ofCell surface (Amsterdam, Netherlands) · 2024Article
- The small molecule CBR-5884 inhibits themBio · 2024Article
- A COmBio · 2024Article
- Baicalin promotes β-1,3-glucan exposure inFrontiers in cellular and infection microbiology · 2024Article
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- P4-ATPase subunit Cdc50 plays a role in yeast budding and cell wall integrity in Candida glabrata.BMC microbiology · 2023Article
- Nature of β-1,3-Glucan-Exposing Features on Candida albicans Cell Wall and Their Modulation.mBio · 2022Article
- Inhibition of fungal pathogenicity by targeting the HScience advances · 2022Article
- Mucosal Infection with Unmasked Candida albicans Cells Impacts Disease Progression in a Host Niche-Specific Manner.Infection and immunity · 2022Article
- Two distinct lipid transporters together regulate invasive filamentous growth in the human fungal pathogen Candida albicans.PLoS genetics · 2022Article
- Impact of changes at theCell surface (Amsterdam, Netherlands) · 2022Article
- Silencing ofJournal of fungi (Basel, Switzerland) · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Candida albicans is among the most common causes of human fungal infections and is an important source of mortality. C. albicans is able to diminish its detection by innate immune cells through masking of β (1,3)-glucan in the inner cell wall with an outer layer of heavily glycosylated mannoproteins (mannan). However, mutations or drugs that disrupt the cell wall can lead to exposure of β (1,3)-glucan (unmasking) and enhanced detection by innate immune cells through receptors like Dectin-1, the C-type signaling lectin. Previously, our lab showed that the pathway for synthesizing the phospholipid phosphatidylserine (PS) plays a role in β (1,3)-glucan masking. The homozygous PS synthase knockout mutant, cho1Δ/Δ, exhibits increased exposure of β (1,3)-glucan. Several Mitogen Activated Protein Kinase (MAPK) pathways and their upstream Rho-type small GTPases are important for regulating cell wall biogenesis and remodeling. In the cho1Δ/Δ mutant, both the Cek1 and Mkc1 MAPKs are constitutively activated, and they act downstream of the small GTPases Cdc42 and Rho1, respectively. In addition, Cdc42 activity is up-regulated in cho1Δ/Δ. Thus, it was hypothesized that activation of Cdc42 or Rho1 and their downstream kinases cause unmasking. Disruption of MKC1 does not decrease unmasking in cho1Δ/Δ, and hyperactivation of Rho1 in wild-type cells increases unmasking and activation of both Cek1 and Mkc1. Moreover, independent hyperactivation of the MAP kinase kinase kinase Ste11 in wild-type cells leads to Cek1 activation and increased β (1,3)-glucan exposure. Thus, upregulation of the Cek1 MAPK pathway causes unmasking, and may be responsible for unmasking in cho1Δ/Δ.
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