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Cell-Cell Communication in Lactic Acid Bacteria
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Emília Maria França Lima, Beatriz Ximena Valencia Quecán, Luciana Rodrigues da Cunha, Bernadette Dora Gombossy de Melo Franco, Uelinton Manoel Pinto
LAB have been playing a significant role in the food industries since they have been used as starter cultures, promoting fermentation and contributing to the sensorial characteristics of the products. Additionally, they are also implicated in increasing the safety and the shelf life of these products by producing metabolites, such as hydrogen peroxide, organic acids and bacteriocins that have an inhibitory effect on the growth of pathogenic microorganisms. Many of these processes are modulated by QS, in a process mediated by signals recognized by a two-component regulatory system that modulates the expression of specific genes as a mechanism of signal transduction. Nisin, a bacteriocin produced by Lactococcus lactis is one of the most studied bacteriocins, and its regulation, like others, depends upon QS. In fact, studies indicate that fermentation of different products is influenced by bacterial interactions and co-cultivation, generally mediated by signaling molecules including AI-2 mediated communication. Even though there are studies demonstrating the importance of QS in LAB, more research is necessary to optimize their potential in food production.
Beneficial Lactic Acid Bacteria
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Besides direct genetic regulation, various factors influence bacteriocin production. The optimal conditions for producing bacterial strains are also favorable for generation of antimicrobial compounds. Temperature, pH, the presence or lack of certain substances were able to affect bacteriocin production (Diep et al. 2000; Li et al. 2002; Leroy and De Vuyst 2005; Van den Berghe et al. 2006). Class I and II bacteriocin regulation relies on signal transduction systems mostly differentiated with regard to peptide inducer. The bacteriocin of class I has a two-component regulatory system activating auto expression. Class II regulation is almost identical to class I regulation pathways, but it is generally associated with peptide pheromone induction as opposed to autoregulation (Snyder and Worobo 2014).
Silver as an Antimicrobial Agent: The Resistance Issue
Published in Huiliang Cao, Silver Nanoparticles for Antibacterial Devices, 2017
Kristel Mijnendonckx, Rob Van Houdt
The silCFBA(orf105)PRSE gene products mediate silver resistance via active efflux and silver sequestration in the periplasm. SilF, a periplasmic chaperone protein, probably transports Ag+ to the SilCBA complex (Figure 7.2). This complex forms a three-polypeptide membrane potential-dependent cation/proton antiporter system that spans the entire cell membrane and belongs to the Heavy Metal Efflux-Resistance Nodulation cell Division (HME-RND) family of efflux. The complex consists of an efflux pump (SilA), an outer membrane factor (SilC) and a membrane fusion protein (SilB) and pumps Ag+ from the periplasm to the exterior of the cell (Franke 2007; Silver 2003). The orf105 gene, coding for a hypothetical protein of 105 aa, was recently reanalysed and was predicted to code for a periplasmic metal chaperone of 146 aa that contains the conserved metal-binding site CxxC and shares 45% protein identity with CopG from Cupriavidus metallidurans CH34 (Randall et al. 2015). SilP is a putative P-type ATPase efflux pump that transports silver ions from the cell cytoplasm to the periplasm (Franke 2007; Silver 2003). However, neither silP nor orf105 is essential for silver resistance as deletion mutants of silP or orf105 or both did not show an increased silver sensitivity (Randall et al. 2015). The transcription of the silCFBA(ORF105aa)P genes is controlled by the two-component regulatory system SilRS, consisting of a transmembrane histidine kinase SilS and a response regulator SilR. This regulatory system is homologous to other two-component regulatory systems involved in the regulation of metal resistance (Franke 2007; Silver 2003). Finally, the silE gene located downstream of silRS, is not controlled by SilRS; nevertheless, transcription is strongly induced in the presence of Ag+ (Silver et al. 1999). SilE codes for a periplasmic protein that shares 48% identity with PcoE, which acts as a ‘metal sponge’ because of its ability to bind multiple Cu+ and Ag+ ions and is encoded by the pcoABCDRSE copper resistance from E. coli plasmid pRJ1004 (Zimmermann et al. 2012). SilE could provide a first line of defense by binding Ag+ before it enters the cytoplasm, as one SilE molecule can bind up to 38 Ag+ ions depending on the experimental conditions (Silver et al. 1999). Additionally, it could act as a chaperone, transporting Ag+ ions to the SilCBA complex either directly or via SilF (Franke 2007; Randall et al. 2015; Silver 2003).
Regulation of flagellar motility and biosynthesis in enterohemorrhagic Escherichia coli O157:H7
Published in Gut Microbes, 2022
Hongmin Sun, Min Wang, Yutao Liu, Pan Wu, Ting Yao, Wen Yang, Qian Yang, Jun Yan, Bin Yang
The two-component regulatory system sensor protein QseC senses EPI/NE and causes autophosphorylation.42 This phosphate is subsequently transferred to the cellular response regulator QseB, and the signals are transmitted to the genome for the differential regulation of signal-sensitive genes. An isogenic qseC mutation in EHEC O157:H7 resulted in reduced flagellin expression and motility compared with the wild-type and complemented strains.43 The qseC mutant showed decreased transcription of flhD, fliA, motA, and fliC, suggesting that qseBC is involved in the transcriptional regulation of flagellar genes. QseBC activates the transcription of flhDC, which is the master regulator of the flagella and motility genes, and, in the absence of flhD, QseBC is unable to activate the transcription of fliA. Further, EMSAs, competition experiments, and DNaseI footprinting analyses showed that the phosphorylated QseB positively regulates EHEC O157:H7 flagellar gene expression by directly interacting with the flhDC regulatory region at the distal high-affinity site and the proximal low-affinity binding sites.44
Virulence-related O islands in enterohemorrhagic Escherichia coli O157:H7
Published in Gut Microbes, 2021
Lingyan Jiang, Wen Yang, Xinlei Jiang, Ting Yao, Lu Wang, Bin Yang
OI-119 is a 3267 bp island (ranging from 3878697 bp to 3881963 bp in the EHEC O157:H7 EDL933 genome), which is highly conserved and widely distributed in all the 143 EHEC O157:H7 strains of 9 clades (Figure 3 and Table S1). OI-119 contains five ORFs (from z4267 to z4271). The z4267 gene (also termed lmiA for low-magnesium-induced regulator A) encodes a putative DNA-binding protein, z4268 and z4269 encode hypothetical proteins of unknown function, whereas z4270 and z4271 encode putative ATP-binding proteins of the ABC transport system. We recently discovered that LmiA, as a novel virulence regulator within OI-119, promoted the bacterial adherence to epithelial cells and expression of LEE genes, facilitating EHEC O157:H7 colonization.75 In contrast, a ΔlmiA mutant exhibited significantly reduced bacterial adherence, as evidenced by bacterial adherence and FAS assays, as well as suppressed the transcriptional and translational expression of LEE genes compared with that of the wild-type. EMSA, ChIP-qPCR, and DNase I footprinting analyses revealed that LmiA directly bound to a 17-base pair motif (5′- TTAAAGTCGTTTGTTAA −3′; −247 to −231 from the ler proximal transcriptional start site) within the LEE1 promoter region to activate the expression of ler, and in turn promote the expression of LEE1-5 genes through Ler. Furthermore, LmiA was reported to be an essential element that integrates the low-magnesium signals from the large intestine into this LEE regulatory network via the PhoP/PhoQ two-component regulatory system.75 This LmiA-mediated virulence regulatory pathway is widely present in a range of EHEC and EPEC serotypes. Disruption of this pathway significantly decreased EHEC O157:H7 adherence in the mouse intestinal tract. Moreover, feeding mice a magnesium-rich diet significantly reduced EHEC O157:H7 adherence in vivo. Therefore, our findings supported the use of magnesium as a dietary supplement and provided greater insights into the dietary cues that can prevent EHEC and EPEC infections in humans.75
Bacteriophages for ESKAPE: role in pathogenicity and measures of control
Published in Expert Review of Anti-infective Therapy, 2021
Amrita Patil, Rajashri Banerji, Poonam Kanojiya, Santosh Koratkar, Sunil Saroj
A strong association has been reported between the expression of lysogeny module, lytic module, and virulence factor, which influence the expression of pathogenicity genes during bacteriophage induction. The lysogeny module encodes integrase (Int, CI) and regulator proteins (Cro). The transition between the lysogenic and lytic life cycle is determined by the expression of int, CI, and Cro proteins. The Int protein assists in the integration of the phage genome in the bacterial chromosome. The expression of CI protein maintains a lysogenic state. However, the expression of Cro triggers the lytic cycle of the phage. Prophage with int gene has been recently found in the epidemic methicillin-resistant Staphylococcus aureus strain. Also, the two-component regulatory system (quorum-sensing system) is found to be involved in the expression of phage-encoded virulence factors such as eta, pvl, scn, and chp. It indicates a close association between the phage life cycle and bacterial virulence. It has been also observed that phage inducing conditions such as exposure to UV, reactive oxygen species, antibiotics, and change in nutrients, pH, temperature increases transcription of the virulence factors that are present in proximity to the lysis module of the phage genome. The methicillin-resistant S. aureus isolated from the skin or soft tissue infection, and necrotizing pneumonia, indicated the role of the lukSf comprising bacteriophages in the pathogenicity of S. aureus. Generally, most of the bacteriophages consist of one virulence factor. However, certain bacteriophages like phiSa3 and phiN315 code for almost five virulence factors. S. aureus bacteriophages Sa3int codes for immune evasion cluster and immune-modulatory proteins such as Chips, Sak, Sea, and Scin that may support the colonization of the strain regardless of the innate immune response [118,119]. Moreover, S. aureus bacteriophages mediate the transfer of SaPIs encoding for toxins and contribute to enhanced pathogenicity of the recipient bacterial cell. The bacteriophage dynamics in the form of transfer of the bacteriophage, duplication, and stable extrachromosomal integration generate heterogeneity within the infecting bacterial population, by regulating the virulence factors and thus increase the pathogenic potential of the whole bacterial consortium [119].