Resolvase-In Vivo Expression Technology Analysis of the<i>Salmonella enterica</i>Serovar Typhimurium PhoP and PmrA Regulons in BALB/c Mice

Merighi, Massimo; Ellermeier, Craig D.; Slauch, James M.; Gunn, John S.

doi:10.1128/jb.187.21.7407-7416.2005

Cited by 74 publications

(80 citation statements)

References 59 publications

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“…This test was important because expression of SPI-2 genes greatly increases upon Salmonella phagocytosis (29,30), and the PmrA/PmrB system is active inside macrophages (11). We found ssaG expression to be ∼30-fold higher at 4 h after internalization by J774A.1 macrophages relative to expression displayed by bacteria grown in LB (Fig.…”

Section: Resultsmentioning

confidence: 70%

“…5C). This result indicates that PmrA is probably activated in response to the signals detected by its cognate sensor PmrB (11). Moreover, it suggests that one of the roles of PhoP in promoting ssrB transcription might be to overcome PmrAdependent repression of ssrB.…”

Section: Discussionmentioning

confidence: 79%

“…The PhoP-activated PmrD protein (9) activates the PmrA protein at the posttranslational level (10). The PmrA/PmrB system is active when Salmonella is inside macrophages and during infection of mice (11). PmrA-dependent modifications of the LPS increase bacterial resistance to the antibiotic polymyxin B (6) and host-derived antimicrobial peptides (6,12), to serum complement (13), and to high concentrations of Fe 3+ (14); and they reduce the proinflammatory properties of the LPS (15).…”

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confidence: 99%

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The lipopolysaccharide modification regulator PmrA limitsSalmonellavirulence by repressing the type three-secretion system Spi/Ssa

Choi

Groisman

2013

Proc. Natl. Acad. Sci. U.S.A.

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The regulatory protein PmrA controls expression of lipopolysaccharide (LPS) modification genes in Salmonella enterica serovar Typhimurium, the etiologic agent of human gastroenteritis and murine typhoid fever. PmrA-dependent LPS modifications confer resistance to serum, Fe 3+ , and several antimicrobial peptides, suggesting that the pmrA gene is required for Salmonella virulence. We now report that, surprisingly, a pmrA null mutant is actually hypervirulent when inoculated i.p. into C3H/HeN mice. We establish that the PmrA protein binds to the promoter and represses transcription of ssrB , a virulence regulatory gene required for expression of the Spi/Ssa type three-secretion system inside macrophages. The pmrA mutant displayed heightened expression of SsrB-dependent genes and faster Spi/Ssa-dependent macrophage killing than wild-type Salmonella . A mutation in the ssrB promoter that abolished repression by the PmrA protein rendered Salmonella as hypervirulent as the pmrA null mutant. The antivirulence function of the PmrA protein may limit the acute phase of Salmonella infection, thereby enhancing pathogen persistence in host tissues.

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Section: Resultsmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 79%

mentioning

confidence: 99%

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The lipopolysaccharide modification regulator PmrA limitsSalmonellavirulence by repressing the type three-secretion system Spi/Ssa

Choi

Groisman

2013

Proc. Natl. Acad. Sci. U.S.A.

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“…In addition, several studies have shown that acid pH also regulates the transcription of certain PhoPQ-regulated genes, mainly conferring protection in exponential phase against inorganic acid stress (Foster, 2000). Thus, Bearson et al (1998) Merighi et al (2005) demonstrated the induction of PhoP in vivo inside macrophages and in the gastrointestinal tract of BALB/c mice, and several studies have shown Salmonella strains harbouring null alleles of the phoP or phoQ gene to be highly attenuated for virulence (Miller et al, 1989;Lee et al, 2007b;Domínguez-Bernal et al, 2008;Karasova et al, 2009). …”

Section: Synthesis Of Acid Shock Proteins (Asps)mentioning

confidence: 99%

Salmonella spp. survival strategies within the host gastrointestinal tract

et al. 2011

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Human salmonellosis infections are usually acquired via the food chain as a result of the ability of Salmonella serovars to colonize and persist within the gastrointestinal tract of their hosts. In addition, after food ingestion and in order to cause foodborne disease in humans, Salmonella must be able to resist several deleterious stress conditions which are part of the host defence against infections. This review gives an overview of the main defensive mechanisms involved in the Salmonella response to the extreme acid conditions of the stomach, and the elevated concentrations of bile salts, osmolytes and commensal bacterial metabolites, and the low oxygen tension conditions of the mammalian and avian gastrointestinal tracts.

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“…The SPC32H lysogen [⌬ LT2 gtrABC1 (32H); SR5100] was isolated by sequential streaking of SPC32H-resistant clones from a lawn of phage-treated ⌬ LT2 gtrABC1 and was verified by PCR amplification of the phage attachment (attR) site. The transcriptional recET:: lacZ fusion was constructed using pCE70, as previously described (26,27). Human influenza virus hemagglutinin (HA) epitope tagging of the specific gene(s) was also accomplished by lambda red recombination using oligonucleotides containing the HA tag sequence.…”

Section: Methodsmentioning

confidence: 99%

Antirepression System Associated with the Life Cycle Switch in the Temperate Podoviridae Phage SPC32H

Kim

Ryu

2013

J Virol

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Prophages switch from lysogenic to lytic mode in response to the host SOS response. The primary factor that governs this switch is a phage repressor, which is typically a host RecA-dependent autocleavable protein. Here, in an effort to reveal the mechanism underlying the phenotypic differences between the Salmonella temperate phages SPC32H and SPC32N, whose genome sequences differ by only two nucleotides, we identified a new class of Podoviridae phage lytic switch antirepressor that is structurally distinct from the previously reported Sipho-and Myoviridae phage antirepressors. The SPC32H repressor (Rep) is not cleaved by the SOS response but instead is inactivated by a small antirepressor (Ant), the expression of which is negatively controlled by host LexA. A single nucleotide mutation in the consensus sequence of the LexA-binding site, which overlaps with the ant promoter, results in constitutive Ant synthesis and consequently induces SPC32N to enter the lytic cycle. Numerous potential Ant homologues were identified in a variety of putative prophages and temperate Podoviridae phages, indicating that antirepressors may be widespread among temperate phages in the order Caudovirales to mediate a prudent prophage induction. B acteriophages (phages), which are natural viral predators of bacteria, multiply by infecting specific host bacteria. Although there is an additional type of phage-host relationship called "steady-state infection," which is exemplified by filamentous phages (1), phage genome replication generally occurs via two different developmental paths: the lytic cycle and the lysogenic cycle. In contrast to the lytic cycle, which results in immediate bursting of the host bacteria and the release of bacteriophage progeny, the lysogenic cycle involves the maintenance of the phage genome as a part of the host genome for several generations, typically by integrating into host chromosomes or, more rarely, by replicating as low-copy-number phage plasmids (2-4). The expression of genes necessary for progeny production and host cell lysis is tightly repressed by a phage regulatory system, but some physiological changes in the host induced by UV light irradiation or other DNA-damaging agents activate the lytic cycle by disabling the phage repressor. Phages fall into two categories: virulent phages that replicate strictly by the lytic cycle and temperate phages that can enter both the lytic cycle and the lysogenic cycle.The lytic switch following lysogenic development has been well studied in the temperate phage lambda. In the lambda lysogenic phase, phage CI repressors form dimers and bind to specific operators to prevent expression of lambda early genes and subsequent late genes (5, 6). Upon host DNA damage, the activated host RecA protein induces CI proteolysis in a manner similar to the inactivation of the host SOS response regulator LexA (7-9). CI proteolysis leads to the expression of early and late genes, resulting in lytic development. This mechanism illustrates how lambda and other similar phages exploit ...

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Resolvase-In Vivo Expression Technology Analysis of theSalmonella entericaSerovar Typhimurium PhoP and PmrA Regulons in BALB/c Mice

Cited by 74 publications

References 59 publications

The lipopolysaccharide modification regulator PmrA limitsSalmonellavirulence by repressing the type three-secretion system Spi/Ssa

The lipopolysaccharide modification regulator PmrA limitsSalmonellavirulence by repressing the type three-secretion system Spi/Ssa

Salmonella spp. survival strategies within the host gastrointestinal tract

Antirepression System Associated with the Life Cycle Switch in the Temperate Podoviridae Phage SPC32H

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