A novel protein, LcrQ, involved in the low-calcium response of Yersinia pseudotuberculosis shows extensive homology to YopH

Rimpiläinen, M; Försberg, Åke; Wolf‐Watz, Hans

doi:10.1128/jb.174.10.3355-3363.1992

Cited by 145 publications

(199 citation statements)

References 45 publications

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“…First the fact that the Y. pseudotuberculosis lcrQ mutant and the Y. enterocolitica yscM1, yscM2 double mutant display a reduction or absence of feedback inhibition when Yop secretion is prevented by Ca 2þ or by a mutation in ysc genes. A second argument would be that overproduction of LcrQ in Y. pseudotuberculosis (Rimpilä inen et al, 1992) and of YscM1 (Allaoui et al, 1995) or YscM2 (this paper) in Y. enterocolitica shuts off Yop synthesis. However, some observations do not fit very well with the regulator hypothesis.…”

Section: Discussionmentioning

confidence: 96%

“…We also demonstrated that the secretion apparatus is installed and functional even when feedback inhibition is maximal, which is very logical. More importantly, we also addressed the question of the difference in phenotype between the yscM mutant of Y. enterocolitica (Allaoui et al, 1995) and the corresponding lcrQ mutant of Y. pseudotuberculosis (Rimpilä inen et al, 1992). We showed that this difference can be explained by our discovery of yscM2, a second gene functionally identical to yscM1 on the pYV plasmid from Y. enterocolitica.…”

Section: Discussionmentioning

confidence: 97%

“…However, some observations do not fit very well with the regulator hypothesis. First, the lcrQ mutant of Y. pseudotuberculosis (Rimpilä inen et al, 1992) and the yscM1, yscM2 double mutant of Y. enterocolitica secrete YopD and LcrV in the presence of Ca 2þ . How would the lack of repressor remove the external stop-valve YopN to open the secretion channel and, if the secretion channel is open, why would the other Yops not be secreted?…”

Section: Discussionmentioning

confidence: 99%

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YscM1 and YscM2, two Yersinia enterocolitica proteins causing downregulation of yop transcription

Stainier

Iriarte

Cornelis

1997

Molecular Microbiology

111

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SummarySynthesis of the Yop proteins by yersiniae is downregulated when secretion is prevented by closure or destruction of the contact (type III) secretion channel. In Yersinia pseudotuberculosis, a mutation in the lcrQ gene, encoding a secreted protein, reduces this feedback inhibition mechanism. Surprisingly, mutation in the yscM gene, the lcrQ homologue in Y. enterocolitica, does not lead to the same deregulated phenotype. In this paper, we addressed the question of this discrepancy. We found a new gene on the Y. enterocolitica pYV plasmid that encodes a protein with 57% identity to YscM (now called YscM1). Overexpression of this gene, called yscM2, like overexpression of lcrQ and yscM1, blocked Yop secretion. A double yscM1, yscM2 mutant had the same phenotype as that of the lcrQ mutant. The discrepancy can thus be explained by the existence of two functionally equivalent copies of yscM in Y. enterocolitica. Overexpression of yscM1 drastically reduced the expression of a yopH-cat reporter gene when tested in a pYV þ background. However, no effect could be observed in the absence of a pYV plasmid, indicating that YscM1 does not act directly as a transcriptional repressor or as an anti-VirF factor. We have also ruled out that YscM acts by obstructing the secretion channel.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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YscM1 and YscM2, two Yersinia enterocolitica proteins causing downregulation of yop transcription

Stainier

Iriarte

Cornelis

1997

Molecular Microbiology

111

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“…Mutants unable to secrete Yops are downregulated for Yop expression (for reviews see Cornelis, 1992;Forsberg et al, 1994b), whereas a yopN mutant, which hypersecretes Yops, is derepressed for Yop expression . LcrQ is a negative regulatory element that was recently shown to be involved in the feedback regulation of Yop expression (Rimpilä inen et al, 1992;Pettersson et al, 1996). Contact between the pathogen and the eukaryotic cell triggers secretion of LcrQ, which results in increased Yop expression (Pettersson et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

YopK of Yersinia pseudotuberculosis controls translocation of Yop effectors across the eukaryotic cell membrane

Holmström

Petterson

Rosqvist

et al. 1997

Molecular Microbiology

127

161

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SummaryIntroduction of anti-host factors into eukaryotic cells by extracellular bacteria is a strategy evolved by several Gram-negative pathogens. In these pathogens, the transport of virulence proteins across the bacterial membranes is governed by closely related type III secretion systems. For pathogenic Yersinia, the protein transport across the eukaryotic cell membrane occurs by a polarized mechanism requiring two secreted proteins, YopB and YopD. YopB was recently shown to induce the formation of a pore in the eukaryotic cell membrane, and through this pore, translocation of Yop effectors is believed to occur (Hå kansson et al., 1996b). We have previously shown that YopK of Yersinia pseudotuberculosis is required for the development of a systemic infection in mice. Here, we have analysed the role of YopK in the virulence process in more detail. A yopK-mutant strain was found to induce a more rapid YopE-mediated cytotoxic response in HeLa cells as well as in MDCK-1 cells compared to the wild-type strain. We found that this was the result of a cell-contact-dependent increase in translocation of YopE into HeLa cells. In contrast, overexpression of YopK resulted in impaired translocation. In addition, we found that YopK also influenced the YopBdependent lytic effect on sheep erythrocytes as well as on HeLa cells. A yopK-mutant strain showed a higher lytic activity and the induced pore was larger

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“…In contrast to the Shigella and Salmonella systems, the VP-encoded TTS system of Yersinia species contains only one transcriptional activator, VirF (also a member of the AraC family) (Cornelis et al, 1998). Furthermore, in Yersinia species, expression of genes encoding both components of the TTS apparatus and effectors is increased under conditions of active secretion (Lambert de Derouvroit et al, 1992;Rimpilainen et al, 1992). The mechanism by which the TTS apparatus activity is transmitted to VirF has not yet been elucidated, but also involves TTS chaperones (Francis et al, 2001;Wulff-Strobel et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Analysis of virulence plasmid gene expression defines three classes of effectors in the type III secretion system of Shigella flexneri

Gall

Mavris

Martino³

et al. 2005

Microbiology

115

174

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Proteins directly involved in entry and dissemination of Shigella flexneri into epithelial cells are encoded by a virulence plasmid of 200 kb. A 30-kb region (designated the entry region) of this plasmid encodes components of a type III secretion (TTS) apparatus, substrates of this apparatus and their dedicated chaperones. During growth of bacteria in broth, expression of these genes is induced at 37 6C and the TTS apparatus is assembled in the bacterial envelope but is not active. Secretion is activated upon contact of bacteria with host cells and is deregulated in an ipaB mutant. The plasmid encodes four transcriptional regulators, VirF, VirB, MxiE and Orf81. VirF controls transcription of virB, whose product is required for transcription of entry region genes. MxiE, with the chaperone IpgC acting as a co-activator, controls expression of several effectors that are induced under conditions of secretion. Genes under the control of Orf81 are not known. The aim of this study was to define further the repertoires of virulence plasmid genes that are under the control of (i) the growth temperature, (ii) each of the known virulence plasmid-encoded transcriptional regulators (VirF, VirB, MxiE and Orf81) and (iii) the activity of the TTS apparatus. Using a macroarray analysis, the expression profiles of 71 plasmid genes were compared in the wild-type strain grown at 37 and 30 6C and in virF, virB, mxiE, ipaB, ipaB mxiE and orf81 mutants grown at 37 6C. Many genes were found to be under the control of VirB and indirectly of VirF. No alteration of expression of any gene was detected in the orf81 mutant. Expression of 13 genes was increased in the secretion-deregulated ipaB mutant in an MxiE-dependent manner. On the basis of their expression profile, substrates of the TTS apparatus can be classified into three categories: (i) those that are controlled by VirB, (ii) those that are controlled by MxiE and (iii) those that are controlled by both VirB and MxiE. The differential regulation of expression of TTS effectors in response to the TTS apparatus activity suggests that different effectors might be required at different times following contact of bacteria with host cells. INTRODUCTIONBacteria of Shigella species are responsible for shigellosis, a human disease characterized by the destruction of the colonic epithelium. Shigellae and enteroinvasive Escherichia coli both contain a virulence plasmid (VP) of approximately 200 kb that encodes most proteins directly involved in entry and dissemination of bacteria into epithelial cells. Sequence analysis of the VP pWR100 (Buchrieser et al., 2000) and its derivative pWR501 (Venkatesan et al., 2001) from a Shigella flexneri strain of serotype 5 and the VP pCP301 (Jin et al., 2002) from an S. flexneri strain of serotype 2a indicated that the VP is composed of a mosaic of approximately 100 genes and numerous insertion sequences. The VP genes exhibit a G+C content from 30 to 60 mol%, suggesting that they were acquired from different sources. The current model of the TTS pathway prop...

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A novel protein, LcrQ, involved in the low-calcium response of Yersinia pseudotuberculosis shows extensive homology to YopH

Abstract: The plasmid-encoded yop genes of pathogenic yersiniae are regulated by the environmental stimuli calcium and temperature. A novel protein, LcrQ, which exhibits a key function in the negative calcium-controlled

Cited by 145 publications

References 45 publications

YscM1 and YscM2, two Yersinia enterocolitica proteins causing downregulation of yop transcription

YscM1 and YscM2, two Yersinia enterocolitica proteins causing downregulation of yop transcription

YopK of Yersinia pseudotuberculosis controls translocation of Yop effectors across the eukaryotic cell membrane

Analysis of virulence plasmid gene expression defines three classes of effectors in the type III secretion system of Shigella flexneri

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