Coordinate Regulation of
            <i>Salmonella</i>
            Pathogenicity Island 1 (SPI1) and SPI4 in
            <i>Salmonella enterica</i>
            Serovar Typhimurium

Main-Hester, Kara L.; Colpitts, Katherine M.; Thomas, Gracie Ann; Fang, Ferric C.; Libby, Stephen J.

doi:10.1128/iai.01224-07

Cited by 83 publications

(93 citation statements)

References 90 publications

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“…If R. insecticola 5.15 directly infects the wasp larva, then it must invade orally through the gut and/or through its cuticle. Different cell types and modes of bacterial infection can result in differential regulation of pathogenicity-related factors, as known for O-antigen adhesions that recognize and attach to specific eukaryotic cells (Jacques 1996), the SPI-1 T3SS that is important for invading certain host cells (Main-Hester et al 2008), and signal-transduction systems such as PhoP-PhoQ (Groisman and Mouslim 2006). One way that bacterial pathogens can achieve virulence is by disabling, resisting, or interfering with their host's innate immune system via T3SS effectors such as YopJ and/or O-antigens.…”

Section: Discussionmentioning

confidence: 99%

Genomic basis of endosymbiont-conferred protection against an insect parasitoid

Hansen¹,

Vorburger²,

Moran³

2011

Genome Res.

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Bacterial endosymbionts exert a variety of beneficial effects on insect hosts. In pea aphids (Acyrthosiphon pisum), several inherited endosymbiont species protect their hosts against parasitoid wasps, which are major natural enemies. However, strains of these symbiont species vary in their ability to confer protection against parasitoids, with some conferring almost complete protection and others conferring almost none. In this study, two strains of the endosymbiont Regiella insecticola (R. insecticola 5.15 and R. insecticola LSR1) were found to differ in ability to protect pea aphids attacked by the parasitoid Aphidius ervi. Parasitism trials reveal that R. insecticola 5.15, but not R. insecticola LSR1, significantly reduced parasitoid success and increased aphid survivorship. To address the potential genetic basis of protection conferred by R. insecticola 5.15 we sequenced the genome of this symbiont strain, and then compared its gene repertoire with that of the already sequenced nonprotective strain R. insecticola LSR1. We identified striking differences in gene sets related to eukaryote pathogenicity. The protective strain R. insecticola 5.15 encoded five categories of pathogenicity factors that were missing or inactivated in R. insecticola LSR1. These included genes encoding the O-antigen biosynthetic pathway, an intact Type 1 Secretion System and its secreted RTX toxins, an intact SPI-1 Type 3 Secretion System and its effectors, hemin transport, and the twocomponent system PhoPQ. These five pathogenicity factors and translocation systems are hypothesized to collectively play key roles in the endosymbiont's virulence against parasitoids, resulting in aphid protection. Mechanisms through which these factors may target parasitoids are discussed.

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Section: Discussionmentioning

confidence: 99%

Genomic basis of endosymbiont-conferred protection against an insect parasitoid

Hansen¹,

Vorburger²,

Moran³

2011

Genome Res.

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“…H-NS has been shown to repress the transcription of hilA, a number of its activators, and other horizontally acquired SPIs (38,46,48,49,53). We hypothesized that the upregulation of hns in the fur-deficient cells may explain the observed Fur-dependent expression of hilA (Fig.…”

Section: Vol 193 2011mentioning

confidence: 99%

“…It has been reported that, in S. Typhimurium, a deletion of hns is lethal, and certain mutations in the alternative sigma factor (rpoS low ) can compensate for this lethality (38,46,53). Therefore, we used P22 transduction to move hilA-lacZ into strains WN153 (rpoS low ) and WN341 (rpoS low ⌬hns) that were derived from 14028s (38,46). We then introduced the ⌬fur mutation into each strain to eliminate Fur expression.…”

Section: Vol 193 2011mentioning

confidence: 99%

Fur Negatively Regulates hns and Is Required for the Expression of HilA and Virulence in Salmonella enterica Serovar Typhimurium

et al. 2011

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Iron is an essential element for the survival of living cells. However, excess iron is toxic, and its uptake is exquisitely regulated by the ferric uptake regulator, Fur. In Salmonella, the Salmonella pathogenicity island 1 (SPI-1) encodes a type three secretion system, which is required for invasion of host epithelial cells in the small intestine. A major activator of SPI-1 is HilA, which is encoded within SPI-1. One known regulator of hilA is Fur. The mechanism of hilA regulation by Fur is unknown. We report here that Fur is required for virulence in Salmonella enterica serovar Typhimurium and that Fur is required for the activation of hilA, as well as of other HilA-dependent genes, invF and sipC. The Fur-dependent regulation of hilA was independent of PhoP, a known repressor of hilA. Instead, the expression of the gene coding for the histone-like protein, hns, was significantly derepressed in the fur mutant. Indeed, the activation of hilA by Fur was dependent on 28 nucleotides located upstream of hns. Moreover, we used chromatin immunoprecipitation to show that Fur bound, in vivo, to the upstream region of hns in a metal-dependent fashion. Finally, deletion of fur in an hns mutant resulted in Fur-independent activation of hilA. In conclusion, Fur activates hilA by repressing the expression of hns.

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“…Activation of the SPI1 rtsA gene only requires the AraC family activators HilC and HilD if both H-NS and Hha are present [64,65]. The SPI1-encoded transcriptional activator HilA not only promotes expression of SPI1 genes but also appears to counter H-NS silencing of the SPI4 pathogenicity island [66], which acts in concert with SPI1 during Salmonella interactions with the host intestinal mucosa [67]. A requirement for the transcriptional activator SsrB for SPI2 expression is reduced in the absence of H-NS, suggesting that SsrB both activates transcription and relieves H-NS-mediated repression [68].…”

Section: Counter-silencing Of H-ns and Its Functional Consequencesmentioning

confidence: 99%

New insights into transcriptional regulation by H-NS

Fang

Rimsky

2008

Current Opinion in Microbiology

186

173

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H-NS, a nucleoid-associated DNA-binding protein of enteric bacteria, was discovered thirty-five years ago and subsequently found to exert widespread and highly pleiotropic effects on gene regulation. H-NS binds to high-affinity sites and spreads along adjacent AT-rich DNA to silence transcription. Preferential binding to sequences with higher AT-content than the resident genome allows H-NS to repress the expression of foreign DNA in a process known as "xenogeneic silencing." Counter-silencing by a variety of mechanisms facilitates the evolutionary acquisition of horizontally transferred genes and their integration into pre-existing regulatory networks. This review will highlight recent insights into the mechanism and biological importance of H-NS-DNA interactions. H-NS--A Nucleoid ProteinH-NS is an abundant DNA-binding protein implicated in the organization of the bacterial chromosome [1]. H-NS and other nucleoid-associated proteins can affect DNA topology at specific loci, thereby modulating gene transcription. Binding by these proteins is proposed to selectively direct supercoiling effects to promoters [2•]. Mutation of hns alters the responsiveness of transcription to changes in DNA superhelicity. Regulatory effects of supercoiling are linked to metabolic and environmental conditions. Thus, H-NS has been viewed as a nucleoid structuring protein with global effects on gene expression [3].H-NS exists primarily as a dimer at low concentrations but can multimerize into higher order complexes [4,5] that form bridges between adjacent DNA helices [6]. Optical tweezers have been used to demonstrate that H-NS dimers or multimers can simultaneously interact with separate DNA binding sites [7••]. H-NS-coated DNA is not self-interactive, suggesting that dimerization or oligomerization must precede DNA binding for bridging to occur. Force measurements suggest that transcription barriers created by H-NS binding are weak (∼7 pN) and readily overcome, so that H-NS oligomers pose only a relative barrier to translocating RNA polymerase. DNA bridging is a conserved feature of H-NS homologs found in most gram-negative bacteria [8] that appears to constrain large DNA loops [9••] and helps to account for the effects of H-NS on transcription. However, it must be noted that the relationship between bridging as a general effect and the silencing of specific promoters is not yet clear.H-NS is more appropriately viewed as a determinant of chromosomal architecture rather than as a general structural component. The analysis of nucleoids treated with urea suggests that *Corresponding Author : Tel 206-275-0966, Fax 206-616-1575, e-mail : fcfang@u.washington.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production proce...

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Coordinate Regulation of Salmonella Pathogenicity Island 1 (SPI1) and SPI4 in Salmonella enterica Serovar Typhimurium

Cited by 83 publications

References 90 publications

Genomic basis of endosymbiont-conferred protection against an insect parasitoid

Genomic basis of endosymbiont-conferred protection against an insect parasitoid

Fur Negatively Regulates hns and Is Required for the Expression of HilA and Virulence in Salmonella enterica Serovar Typhimurium

New insights into transcriptional regulation by H-NS

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