Bile‐induced peptidoglycan remodelling in <scp><i>S</i></scp><i>almonella enterica</i>

Hernández, Sara B.; Cava, Felipe; Pucciarelli, M. Graciela; Portillo, Francisco García‐del; Pedro, Miguel A. de; Casadesús, Josep

doi:10.1111/1462-2920.12491

Cited by 29 publications

(30 citation statements)

References 68 publications

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“…It has previously been reported that amidase-deficient E. coli is also sensitive to components of bile and other agents, which is thought to reflect weakness of the outer membrane (9). Resistance against bile has been previously linked to cell envelope structures, such as lipopolysaccharide (38), and to reduced levels of PG-bound lipoprotein (39,40). Since NlpD is predicted to be an outer membrane protein, it may contribute to the release of Lpp-bound peptides by preferentially activating AmiB near outer-membrane-proximal PG.…”

Section: Discussionmentioning

confidence: 99%

“…However, many studies have demonstrated that PG synthesis is highly responsive to environmental conditions. For example, changes in PG composition and altered PG synthase activity contribute to bile resistance in Salmonella enterica (39,41) and PG composition changes during stationary phase (42). Pathogenic bacteria can also remodel PG to avoid a host response (5,(43)(44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

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Cell Separation in Vibrio cholerae Is Mediated by a Single Amidase Whose Action Is Modulated by Two Nonredundant Activators

et al. 2014

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Synthesis and hydrolysis of septal peptidoglycan (PG) are critical processes at the conclusion of cell division that enable separation of daughter cells. Cleavage of septal PG is mediated by PG amidases, hydrolytic enzymes that release peptide side chains from the glycan strand. Most gammaproteobacteria, including Escherichia coli, encode several functionally redundant periplasmic amidases. However, members of the Vibrio genus, including the enteric pathogen Vibrio cholerae, encode only a single PG amidase, AmiB. Here, we show that V. cholerae AmiB is crucial for cell division and growth. Genetic and biochemical analyses indicated that AmiB is regulated by two activators, EnvC and NlpD, at least one of which is required for AmiB's localization to the cell division site. Localization of the activators (and thus of AmiB) is dependent upon the cell division protein FtsN. These factors mediate septal PG cleavage in E. coli as well; however, their precise roles vary between the two organisms in a number of ways. Notably, even though V. cholerae EnvC and NlpD appear to be functionally redundant under most growth conditions tested, NlpD is specifically required for intestinal colonization in the infant mouse model of cholera and for V. cholerae resistance against bile salts, perhaps due to environmental regulation of AmiB or its activators. Collectively, our findings reveal that although the cellular components that enable cleavage of septal PG appear to be generally conserved between E. coli and V. cholerae, they can be combined into diverse functional regulatory networks.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cell Separation in Vibrio cholerae Is Mediated by a Single Amidase Whose Action Is Modulated by Two Nonredundant Activators

et al. 2014

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“…Bile resistance can be studied under laboratory conditions by supplementing microbiological culture media with either ox bile or individual bile salts (Pace et al ., ; Van Velkinburgh and Gunn, ; Raphael et al ., ; Froelich et al ., ; Malik‐Kale et al ., ; Casadesús et al ., ; Lertpiriyapong et al ., ). Using this reductionist approach, genetic and biochemical analysis has permitted the identification of cell components and mechanisms involved in bacterial resistance to bile (Gunn, ; Casadesús et al ., ; Hernández et al ., ). Examples include envelope structures like the lipopolysaccharide (Picken and Beacham, ; Van Velkinburgh and Gunn, ; Murata et al ., ; Crawford et al ., ; Hernández et al ., ; May and Groisman, ) and the enterobacterial common antigen (Ramos‐Morales et al ., ), which serve as barriers that reduce intake of bile salts.…”

Section: Introductionmentioning

confidence: 99%

“…Downregulation of genes encoding porins (Hernández et al ., ) may also reduce intake of bile salts. In turn, peptidoglycan remodelling may permit bile‐insensitive cell wall synthesis (Hernández et al ., ). However, envelope barriers are insufficient to prevent bile intake, and the activity of efflux pumps is necessary to prevent intracellular accumulation of bile salts (Thanassi et al ., ; Piddock, ).…”

Section: Introductionmentioning

confidence: 99%

Adaptation of Salmonella enterica to bile: essential role of AcrAB‐mediated efflux

Urdaneta

Casadesús

2018

Environmental Microbiology

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Adaptation to bile is the ability to endure the lethal effects of bile salts after growth on sublethal concentrations. Surveys of adaptation to bile in Salmonella enterica ser. Tyhimurium reveal that active efflux is essential for adaptation while other bacterial functions involved in bile resistance are not. Among S. enterica mutants lacking one or more efflux systems, only strains lacking AcrAB are unable to adapt, thus revealing an essential role for AcrAB. Transcription of the acrAB operon is upregulated in the presence of a sublethal concentration of sodium deoxycholate (DOC) while other efflux loci are either weakly upregulated or irresponsive. Upregulation of acrAB transcription is strong during exponential growth, and weak in stationary cultures. Single cell analysis of ethidium bromide accumulation indicates that DOC-induced AcrAB-mediated efflux occurs in both exponential and stationary cultures. Upregulation of acrAB expression may thus be crucial at early stages of adaptation, while sustained AcrAB activity may be sufficient to confer bile resistance in nondividing cells.

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“…Two components of the outer membrane are important for bile resistance: the LPS (Crawford et al, 2012;Gunn, 2000) and the enterobacterial common antigen (ECA) (Ramos-Morales et al, 2003). Recently, it has been shown that exposure to the bile salt sodium deoxycholate is associated with changes in the structure of the second layer of the cell envelope, the PG, and that PG remodelling contributes to bile resistance (Hernández et al, 2015). Once bile enters the cell, additional mechanisms are activated.…”

Section: Bilementioning

confidence: 99%