Salmonella typhimurium secreted invasion determinants are homologous to Shigella lpa proteins

205

170

Bacterial pathogens have evolved sophisticated mechanisms to interact with their hosts. A specialized type III protein secretion system capable of translocating bacterial proteins into host cells has emerged as a central factor in the interaction between a variety of mammalian and plant pathogenic bacteria with their hosts. Here we describe AvrA, a novel target of the centisome 63 type III protein secretion system of Salmonella enterica. AvrA shares sequence similarity with YopJ of the animal pathogen Yersinia pseudotuberculosis and AvrRxv of the plant pathogen Xanthomonas campestris pv. vesicatoria. These proteins are the first examples of putative targets of type III secretion systems in animal and plant pathogenic bacteria that share sequence similarity. They may therefore constitute a novel family of effector proteins with related functions in the cross-talk of these pathogens with their hosts.

Section: Resultsmentioning

confidence: 99%

A secreted Salmonella protein with homology to an avirulence determinant of plant pathogenic bacteria

Hardt

Galán

1997

205

170

“…Our finding is consistent with the observation that many Hrp proteins are structurally related to those that participate in the construction of bacterial flagella (23), suggesting an involvement of Hrp proteins in the assembly of an extracellular macromolecular structure. Salmonella, Shigella, and Yersinia, all of which contain type III secretion systems, secrete proteins required for pathogenesis (47)(48)(49)(50)(51). Both Salmonella typhimurium and Shigella flexneri are enteroinvasive pathogens.…”

Section: Discussionmentioning

confidence: 99%

Hrp pilus: An hrp -dependent bacterial surface appendage produced by Pseudomonas syringae pv. tomato DC3000

Roine

Wei

Yuan

et al. 1997

327

279

Hypersensitive response and pathogenicity (hrp) genes control the ability of major groups of plant pathogenic bacteria to elicit the hypersensitive response (HR) in resistant plants and to cause disease in susceptible plants. A number of Hrp proteins share significant similarities with components of the type III secretion apparatus and f lagellar assembly apparatus in animal pathogenic bacteria. Here we report that Pseudomonas syringae pv. tomato strain DC3000 (race 0) produces a filamentous surface appendage (Hrp pilus) of 6-8 nm in diameter in a solid minimal medium that induces hrp genes. Formation of the Hrp pilus is dependent on at least two hrp genes, hrpS and hrpH (recently renamed hrcC), which are involved in gene regulation and protein secretion, respectively. Our finding of the Hrp pilus, together with recent reports of Salmonella typhimurium surface appendages that are involved in bacterial invasion into the animal cell and of the Agrobacterium tumefaciens virB-dependent pilus that is involved in the transfer of T-DNA into plant cells, suggests that surface appendage formation is a common feature of animal and plant pathogenic bacteria in the infection of eukaryotic cells. Furthermore, we have identified HrpA as a major structural protein of the Hrp pilus. Finally, we show that a nonpolar hrpA mutant of P. syringae pv. tomato DC3000 is unable to form the Hrp pilus or to cause either an HR or disease in plants.Major groups of Gram-negative plant pathogenic bacteria belonging to genera Erwinia, Pseudomonas, Ralstonia, and Xanthomonas contain hypersensitive reaction and pathogenicity (hrp) genes. These genes control the ability of these bacteria to initiate interactions with plants, including elicitation of the hypersensitive reaction (HR), characterized by rapid localized death of plant cells at the pathogen infection site in resistant plants and causation of disease in susceptible plants (1, 2).hrp genes of Pseudomonas syringae are expressed in planta as a result of a regulatory cascade involving the gene products of hrpS and hrpR, positive transcriptional regulators, and of hrpL, an alternative sigma factor (3, 4). HrpL recognizes a consensus sequence motif (''harp box'') that has been identified in the upstream regions of many hrp and avr genes (4). The expression of hrp genes of many P. syringae pathovars can also be induced in vitro when bacteria are grown in defined minimal medium with low pH and containing certain sugars or sugar alcohols as carbon sources (5-7).The 25-kb hrp͞hrmA gene cluster of Pseudomonas syringae pv. syringae strain 61 is sufficient to enable nonpathogenic strains of Pseudomonas fluorescens and Escherichia coli to elicit the HR in nonhost plants (8). Sixteen of the 25 genes in this completely sequenced hrp͞hrmA gene cluster are either predicted or shown to be required for secretion of harpin Pss , a proteinaceous elicitor of the HR encoded by hrpZ (9, 10). Nine of these hrp genes, recently renamed hrc genes (11), are broadly conserved among P. syringae pathovars, Erwi...

“…Strain VV 341 (ref. 15; hilA::kan-334) was used as a source for the hilA-inactivating mutation, and Escherichia coli LM106 (16) was used as a source for pnp::Tn5, and the resistance elements were transferred by phage transduction. Strains were grown in LB or on Luria agar with antibiotics as appropriate.…”

Section: Methodsmentioning

confidence: 99%

Polynucleotide phosphorylase is a global regulator of virulence and persistency in Salmonella enterica

Clements

Eriksson

Thompson

et al. 2002

154

133

For many pathogens, the ability to regulate their replication in host cells is a key element in establishing persistency. Here, we identified a single point mutation in the gene for polynucleotide phosphorylase (PNPase) as a factor affecting bacterial invasion and intracellular replication, and which determines the alternation between acute or persistent infection in a mouse model for Salmonella enterica infection. In parallel, with microarray analysis, PNPase was found to affect the mRNA levels of a subset of virulence genes, in particular those contained in Salmonella pathogenicity islands 1 and 2. The results demonstrate a connection between PNPase and Salmonella virulence and show that alterations in PNPase activity could represent a strategy for the establishment of persistency.T he species Salmonella enterica is a classic example of the facultative intracellular pathogen that can cause acute and persistent infections (1-4). Typhoid fever is a serious manifestation of systemic salmonellosis in humans and involves an estimated 16.6 million new cases per year (2) with between 2% and 5% of the cases developing into the carrier state (3, 4).Much of the knowledge of salmonellosis pathogenesis comes from work on the murine salmonellosis model (1, 5), and this model has been used to define bacterial virulence factors (1, 6, 7). An important virulence trait of Salmonella is its ability to invade and grow within host cells, and many of the genetic determinants essential for these processes have been well characterized (8-11). Invasion of epithelial cells requires the expression of a type III secretion apparatus, which translocates effector proteins from the bacterium to the host cell, inducing the cell to internalize the bacteria by bacterial-mediated endocytosis (8,11). Proteins involved in this process are encoded by a large cluster of genes collectively termed Salmonella pathogenicity island 1 (SPI 1). The ability to grow intracellularly, once internalized within the host cell, requires the coordinate expression of additional sets of virulence factors (6), such as SPI 2 (1, 10).Although chronic carriage of Salmonella is recognized as a significant complication that facilitates spread of the disease (2) and predisposes victims to additional clinical conditions (12, 13) the mechanism underlying persistency has remained poorly understood. We discovered the link between polynucleotide phosphorylase (PNPase) and chronic infection while characterizing a mutant of Salmonella typhimurium that was defective in its expression of virulence-associated AgfA fimbriae and known to establish persistent infection in BALB͞c mice (14). Materials and Methods Mapping and Sequencing of MC2 Mutation.A random Tn10camd insertion library from S. typhimurium 14028 (22) was transduced into MC1 by P22 transduction selecting for chloramphenicolresistant colonies. Transductants were pooled and used to propagate phage KB1, which was then used to transduce MC2. Chloramphenicol-resistant colonies were screened for agf expression on Congo red pla...