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The majority of chronic infections involve a biofilm stage. In most bacteria, the synthesis of the ubiquitous second messenger cyclic diGMP (cdiGMP) represents a typical principle inside the formation of otherwise very diverse and speciesspecific biofilms [1]. For that reason, cdiGMP signaling pathways play a key function in chronic infections [4]. The human pathogen Pseudomonas aeruginosa is accountable for a plethora of biofilmmediated chronic infections among which cystic fibrosis (CF) pneumonia would be the most frightening [5]. Through longterm colonization of CF lungs P. aeruginosa undergoes particular genotypic adaptation to the host environment and, immediately after a yearlong persistence, it developssmallcolony variants (SCVs) [6]. SCVs, which display higher intracellular cdiGMP levels [91], are characterized by enhanced biofilm formation, higher fimbrial expression, repression of flagellar genes, resistance to phagocytosis, and enhanced antibiotic resistance [104]; their appearance correlates with a poor patient clinical outcome [6,12,15]. A direct connection in between the presence of bacterial persister cells along with the recalcitrant nature of chronic infections has been proposed [16]. The cdiGMP metabolism in P. aeruginosa is highly complicated: 42 genes containing putative diguanylate cyclases (DGCs) and/or phosphodiesterase are present [17].838882-52-3 web It has been shown that SCVs generated in vitro as well as obtained from clinical isolates include mutations that upregulate the activity ofPLOS 1 | www.Price of 1885090-83-4 plosone.PMID:33491569 orgGGDEF Domain Structure of YfiN from P. aeruginosaa precise DGC, i.e. YfiN (also called TpbB [18], encoded by the PA1120 gene), suggesting a key part of this enzyme. Because YfiN is definitely the effector protein of a tripartite signaling module YifBNR [14,19,20], in this work we decide to make use of the name YfiN for coherence with the other two members with the operon PA1119 and PA1121, which, inside the Pseudomonas genome database (http://www.pseudomonas.com/), are named YfiB and YfiR, respectively. Formation of SCVs depends on enhanced cdiGMP output by YfiN, which elevates transcription of the pel operon [11,14,21]. The YfiBNR system most likely contributes for the degree of persistence of P. aeruginosa cells in CF lungs. Jenal and coworkers [20], have shown, by taking a look at mutations inside the YfiBNR genes identified in clinical strains of P. aeruginosa, that the activity of YfiN (and also the occurrence in the SCV phenotype) is.
