Biofilm matrix regulation by Candida albicans Zap1
Ontology highlight
ABSTRACT:
ORGANISM(S): Candida albicans
PROVIDER: GSE29785 | GEO | 2011/06/09
SECONDARY ACCESSION(S): PRJNA141061
REPOSITORIES: GEO
Similar Datasets
Project description:The Zap1 ChIP-chips were performed in a/alpha cell types using C-terminally Myc-tagged proteins and Myc antibodies. ChIPs were performed on 48 hour biofilm cells grown in Spider medium. Two biological replicates were performed, and normalized data is reported in matrix. Myc tagged strains were compared to untagged control strains.
2011-06-09 | E-GEOD-29785 | biostudies-arrayexpress
Project description:The planktonic versus biofilm gene expression arrays were performed in a/alpha cell types. Gene expression arrays were performed on planktonic vs biofilm cells grown in Spider medium at 37C. Normalized data is reported in matrix.
2011-07-08 | GSE30474 | GEO
Project description:The planktonic versus biofilm gene expression arrays were performed in a/alpha cell types. Gene expression arrays were performed on planktonic vs biofilm cells grown in Spider medium at 37C. Normalized data is reported in matrix. Biofilm strains (48 hour biofilms) were compared to planktonic strains (log phase planktonic cells) in Spider medium at 37C.
2011-07-08 | E-GEOD-30474 | biostudies-arrayexpress
Project description:Transcriptional profiling of Candida glabrata zap1Δ and zap1Δ::ZAP1 strains, comparing cells grown under planktonic and biofilm-inducing conditions. Goal was to analyse the effect of ZAP1 deletion in the transcriptomic profile of C. glabrata biofilm cells (in comparision to planktonic cells), under acidic conditions, in order to study the function of the Zap1 transcription factor in C. glabrata biofilm matrix production.
2024-08-08 | GSE226915 | GEO
Project description:The vaginal acidic environment potentiates the formation of Candida glabrata biofilms, leading to complicated and recurrent infections. Importantly, the regulation of biofilm matrix is known to contribute to the recalcitrant features of Candida biofilms. In this study we reveal a new matrix regulator of C. glabrata acidic biofilms, Zap1, and analyzed its modulation of the transcriptome (by microarrays) and matrix proteome (by LC-MS/MS). For that, the deletion mutant zap1Δ and its complemented strain zap1Δ::ZAP1 were constructed and their biofilms were developed at pH 4 (adjusted with lactic acid). The results revealed that Zap1 is a negative regulator of the total amount of protein and carbohydrate in the biofilm matrix. Accordingly, various genes and matrix proteins with predicted functions in the regulation of carbohydrate metabolism, sugar binding, sugar transport and adhesion (including Epa family) were found to be repressed by Zap1. Nevertheless, the results also suggested that Zap1 is essential to the delivery and organization of some matrix components. Indeed, Zap1 was required to the secretion of 122 proteins to the matrix and induced the expression of 557 genes, including various targets involved in glucan-metabolism. Additionally, Zap1 induced targets with roles in virulence, resistance to antifungals and host immunity evasion, including yapsins, ERG family and moonlighting proteins. Zap1 was also required to the secretion of acidic-specific matrix proteins, indicating a contribution to the response to the acidic environment. Overall, this study demonstrates that Zap1 is a relevant regulator of biofilm matrix, contributing to a better understanding of C. glabrata acidic biofilms.
2024-10-28 | PXD044153 | Pride
Project description:A biofilm is a surface-associated population of microorganisms embedded in a matrix of extracellular polymeric substances. Biofilms are a major natural growth form of microorganisms and the cause of pervasive device-associated infection. This report focuses on the biofilm matrix of Candida albicans, the major fungal pathogen of humans. We report here that the C. albicans zinc-response transcription factor Zap1 is a negative regulator of a major matrix component, soluble beta-1,3 glucan, in both in vitro and in vivo biofilm models. To understand the mechanistic relationship between Zap1 and matrix, we identified Zap1 target genes through expression profiling and full genome chromatin immunoprecipitation. On the basis of these results, we designed additional experiments showing that two glucoamylases, Gca1 and Gca2, have positive roles in matrix production and may function through hydrolysis of insoluble beta-1,3 glucan chains. We also show that a group of alcohol dehydrogenases Adh5, Csh1, and Ifd6 have roles in matrix production: Adh5 acts positively, and Csh1 and Ifd6, negatively. We propose that these alcohol dehydrogenases generate quorum-sensing aryl and acyl alcohols that in turn govern multiple events in biofilm maturation. Our findings define a novel regulatory circuit and its mechanism of control of a process central to infection.
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Project description:Biofilm matrix regulation by Candida albicans Zap1
| PRJNA141061 | ENA
Project description:Cells from all kingdoms of life produce extracellular vesicles (EVs). Their cargo is protected from the environment by the surrounding lipid bilayer. EVs from many organisms have been shown to function in cell-cell communication, relaying signals that impact metazoan development, microbial quorum sensing, and pathogenic host-microbe interactions. Here, we have investigated the production and functional activities of EVs in a surface-associated microbial community or biofilm of the fungal pathogen Candida albicans. Crowded communities like biofilms are a context in which EVs are likely to function. Biofilms are noteworthy because they are encased in an extracellular polymeric matrix and because biofilm cells exhibit extreme tolerance to antimicrobial compounds. We found that biofilm EVs are distinct from those produced by free-living planktonic cells and display strong parallels in composition to biofilm matrix material. The functions of biofilm EVs were delineated with a panel of mutants defective in orthologs of endosomal sorting complexes required for transport (ESCRT) subunits, which are required for normal EV production in diverse eukaryotes. Most ESCRT-defective mutations caused reduced biofilm EV production, reduced matrix polysaccharide levels, and greatly increased sensitivity to the antifungal drug fluconazole. Matrix accumulation and drug hypersensitivity of ESCRT mutants were reversed by addition of wild-type (WT) biofilm EVs. Vesicle complementation showed that biofilm EV function derives from specific cargo proteins. Our studies indicate that C. albicans biofilm EVs have a pivotal role in matrix production and biofilm drug resistance. Biofilm matrix synthesis is a community enterprise; prior studies of mixed cell biofilms have demonstrated extracellular complementation. Therefore, EVs function not only in cell-cell communication but also in the sharing of microbial community resources.
| S-EPMC6209495 | biostudies-literature
Project description:Biofilm-associated polymicrobial infections, particularly those involving fungi and bacteria, are responsible for significant morbidity and mortality and tend to be challenging to treat. Candida albicans and Staphylococcus aureus specifically are considered leading opportunistic fungal and bacterial pathogens, respectively, mainly due to their ability to form biofilms on catheters and indwelling medical devices. However, the impact of mixed-species biofilm growth on therapy remains largely understudied. In this study, we investigated the influence of C. albicans secreted cell wall polysaccharides on the response of S. aureus to antibacterial agents in biofilm. Results demonstrated significantly enhanced tolerance for S. aureus to drugs in the presence of C. albicans or its secreted cell wall polysaccharide material. Fluorescence confocal time-lapse microscopy revealed impairment of drug diffusion through the mixed biofilm matrix. Using C. albicans mutant strains with modulated cell wall polysaccharide expression, exogenous supplementation, and enzymatic degradation, the C. albicans-secreted ?-1,3-glucan cell wall component was identified as the key matrix constituent providing the bacteria with enhanced drug tolerance. Further, antibody labeling demonstrated rapid coating of the bacteria by the C. albicans matrix material. Importantly, via its effect on the fungal biofilm matrix, the antifungal caspofungin sensitized the bacteria to the drugs. Understanding such symbiotic interactions with clinical relevance between microbial species in biofilms will greatly aid in overcoming the limitations of current therapies and in defining potential new targets for treating polymicrobial infections.The fungus Candida albicans and the bacterium Staphylococcus aureus are important microbial pathogens responsible for the majority of infections in hospitalized patients and are often coisolated from a host. In this study, we demonstrated that when grown together, the fungus provides the bacterium with enhanced tolerance to antimicrobial drugs. This process was mediated by polysaccharides secreted by the fungal cell into the environment. The biofilm matrix formed by these polysaccharides prevented penetration by the drugs and provided the bacteria with protection. Importantly, we show that by inhibiting the production of the fungal polysaccharides, a specific antifungal agent indirectly sensitized the bacteria to antimicrobials. Understanding the therapeutic implications of the interactions between these two diverse microbial species will aid in overcoming the limitations of current therapies and in defining new targets for treating complex polymicrobial infections.
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Project description:ChIP-chip to determine the regulation of the K. lactis hsgs (ChIP of MATa1, MATalpha2, and RME1). The MATa1 and MATalpha2 ChIPs were performed in an a/alpha cell using N-terminally HA-tagged proteins and the RME1 ChIPs were perfomed in an a cell using C-terminally myc-tagged protein. For the RME1 ChIPs, the cells grown with out phosphate. For the MATa1 andMATalpha2 ChIPs the cells were grown in YEPD.
2010-12-01 | GSE25209 | GEO