Sharing the Burden to Build a Matrix
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RESEARCH HIGHLIGHTS BIOFILMS IN BRIEF Sharing the burden to BACTERIAL GENETICS ppGpp triggers the switch build a matrix Riboswitches are highly structured, non-coding RNA elements located upstream of the coding region of bacterial mRNAs. Biofilms are structured consortia costly to produce and are shared They bind cellular ligands via their aptamer domain to regulate of bacteria embedded in a self- amongst the community. Using gene expression of the adjacent gene or operon through produced extracellular matrix Δeps and ΔtasA mutants in growth their expression platform domain. Five riboswitch classes (ECM) of exopolysaccharides (EPSs), competition assays, they observed a have been identified that sense nucleotide-based signalling molecules, including c-di-GMP and c-di-AMP. This study structural proteins and extracellular significant fitness cost of EPSs and describes a riboswitch class that selectively binds the alarmone DNA. As the production of the TasA production. In agreement with guanosine tetraphosphate (ppGpp). Binding of ppGpp to ECM is metabolically costly, it has previous observations, they found candidate riboswitches induced structural changes in the been suggested that the overall that Δeps and ΔtasA mutants could RNA, and gene expression was regulated via transcription metabolic cost to the community not establish biofilms in monoculture, termination. Riboswitches for ppGpp may regulate genes may be reduced by allocating ECM but could when they were co-cultured involved in branched-chain amino acid biosynthesis, genes production to a subpopulation of or if conditioned media from encoding glutamate synthase domains and operons containing ATP-binding cassette transporters. cells. In a recent study, Dragoš et al. producers was added, indicating that ORIGINAL ARTICLE Sherlock, M. E., Sudarsan, N. & Breaker, R. R. Riboswitches for the investigate the benefits of division EPSs and TasA can be shared. alarmone ppGpp expand the collection of RNA-based signaling systems. Proc. Natl Acad. of labour during ECM production The authors hypothesised that Sci. https://doi.org/10.1073/pnas.1720406115 (2018) and show that both genetic and phenotypic differentiation into EPS phenotypic strategies for a division producers and TasA producers could FUNGAL PATHOGENESIS of labour promote biofilm formation. occur within B. subtilis pellicles. Using Bacillus subtilis pellicle Using confocal laser scanning Breaking barriers (a floating biofilm at an air-liquid microscopy and cells expressing Candida albicans asymptomatically colonizes healthy interface) formation as a model fluorescent markers under the individuals, but it is also an opportunistic pathogen that system, the authors observed that control of the ECM gene promoters, can translocate across the intestinal epithelium and cause bloodstream infections. Using in vitro cell culture models, the two major ECM components — they observed heterogeneity in the Allert, Förster et al. show that translocation through an intact EPSs and TasA — are metabolically expression of eps and tasA within intestinal barrier is initiated by invasion and followed by cellular damage and loss of epithelial integrity. Translocation occurs mainly via a transcellular route, which causes necrotic BACTERIAL PATHOGENESIS epithelial damage. The cytolytic peptide toxin of C. albicans, candidalysin, was found to be essential for damage of enterocytes and was a key factor in fungal translocation. Falling into your own trap However, fungal invasion and low-level translocation can also Staphylococcus aureus is an important The authors used a CRISPR-Cas9 occur in a candidalysin-independent manner — possibly by bacterial pathogen that can cause screen in human macrophages and passing through intercellular spaces. serious invasive infections in found that cells that lacked genes ORIGINAL ARTICLE Allert, S. & Förster, T. M. et al. Candida albicans-induced epithelial damage mediates translocation through intestinal barriers. mBio 9, e00915-18 (2018) humans. The first line of defence that encode human equilibrative against invasive S. aureus involves transporter 1 (hENT1, which mediates the recruitment of neutrophils, uptake of nucleosides and of nucleoside SYMBIOSIS which release extracellular traps derivatives) and kinases of the purine (termed NETs, which are composed of salvage pathway (adenosine kinase Four is a crowd chromatin, proteases and antimicrobial (ADK) and deoxycytidine kinase (DCK)) Acromyrmex leafcutter ants form a tripartite symbiosis peptides) that capture microorganisms were resistant to dAdo. with the fungal cultivar Leucoagaricus gongylophorus and and enable their elimination by Although dAdo was found in the Pseudonocardia bacteria. Ants provide leaves as growth substrate for the fungus and the fungus provides the sole food macrophage-mediated phagocytosis. cytoplasm of control cells, dAdo could source for ant larvae. The bacteria produce molecules that To escape clearance, S. aureus not be detected in the cytoplasm of protect the cultivar against pathogens, such as the fungal degrades NETs, which is associated mutant cells that lacked the membrane parasite Escovopsis weberi. Two studies show that E. weberi with the formation of cytotoxic protein hENT1, which suggests that produces secondary metabolites during infection of the deoxyadenosine (dAdo) by S. aureus hENT1 transports dAdo across the cultivar that promote the collapse of the fungus garden in nuclease and adenosine synthase A. plasma membrane. Furthermore, leafcutter ant colonies. Heine et al. identified melinacidin IV Previous work showed that dAdo inhibition of ADK and DCK decreased and the terpene-indole alkaloid shearinine D, both of which induces apoptosis in macrophages and dAdo-mediated apoptosis of kill Pseudonocardia species. Ingestion of shearinine D by ants thus promotes persistent infection; macrophages, which is in agreement adversely affects their behaviour and results in ant death. with a role of those kinases in dAdo Dhodary et al. showed that E. weberi produces shearinine L however, the underlying mechanism and shearinine M, as well as emodin and cycloarthropsone, was not clear. This study reports intoxication. which inhibit the growth of L. gongylophorous. that dAdo-mediated macrophage Moreover, the authors were able ORIGINAL ARTICLES Heine, D. et al. Chemical warfare between leafcutter ant symbionts apoptosis involves a macrophage to show that ADK and DCK catalyze and a co-evolved pathogen. Nat. Comms. 9, 2208 (2018). | Dhodary, B. et al. Secondary membrane transporter and kinases of the conversion of dAdo to dAMP metabolites from Escovopsis weberi and their role in attacking the garden fungus of leaf the purine salvage pathway. for the subsequent synthesis of dADP cutting ants. Chem. Eur. J. 24, 4445–4452 (2018) 454 | AUGUST 2018 | VOLUME 16 www.nature.com/nrmicro © 2018 Macmillan Publishers Limited, part of Springer Nature. All rights reserved..