Evaluation of Protective Immunity Induced by Yersinia enterocolitica Type-III Secretion System Mutants

Author(s):  
Emanuelle Mamroud ◽  
Yehuda Flashner ◽  
Avital Tidhar ◽  
Raphael Ber ◽  
David Gur ◽  
...  
2006 ◽  
Vol 75 (3) ◽  
pp. 1512-1516 ◽  
Author(s):  
Camino Pérez-Gutiérrez ◽  
Catalina M. Llompart ◽  
Mikael Skurnik ◽  
José A. Bengoechea

ABSTRACT We show that the expression of a Yersinia enterocolitica O:8 pYV-encoded type III secretion system was altered in a rough mutant (YeO8-R) due to elevated levels of FlhDC. H-NS might underlie flhDC upregulation in YeO8-R, and the data suggest a relationship between the absence of O antigen and the expression of H-NS.


2013 ◽  
Vol 81 (7) ◽  
pp. 2478-2487 ◽  
Author(s):  
Kimberly A. Walker ◽  
Vivien I. Maltez ◽  
Joshua D. Hall ◽  
Nicholas P. Vitko ◽  
Virginia L. Miller

ABSTRACTThe highly pathogenicYersinia enterocoliticastrains have a chromosomally encoded type III secretion system (T3SS) that is expressed and functionalin vitroonly when the bacteria are cultured at 26°C. Mutations that render this system nonfunctional are slightly attenuated in the mouse model of infection only following an oral inoculation and only at early time points postinfection. The discrepancy between the temperature required for the Ysa gene expression and the physiological temperature required for mammalian model systems has made defining the role of this T3SS challenging. Therefore, we explored the use ofDrosophilaS2 cells as a model system for studying Ysa function. We show here thatY. enterocoliticais capable of infecting S2 cells and replicating intracellularly to high levels, an unusual feature of this pathogen. Importantly, we show that the Ysa T3SS is required for robust intracellular replication. A secretion-deficient mutant lacking the secretin gene,ysaC, is defective in replication within S2 cells, marking the first demonstration of a pronounced Ysa-dependent virulence phenotype. Establishment of S2 cells as a model forY. enterocoliticainfection provides a versatile tool to elucidate the role of the Ysa T3SS in the life cycle of this gastrointestinal pathogen.


2016 ◽  
Vol 198 (12) ◽  
pp. 1725-1734
Author(s):  
Kimberly A. Walker ◽  
Lauren A. Griggs ◽  
Markus Obrist ◽  
Addys Bode ◽  
R. Patrick Summers ◽  
...  

ABSTRACTTheYersinia enterocoliticaYsa type III secretion system (T3SS) is associated with intracellular survival, and, like other characterized T3SSs, it is tightly controlled. Expression of theysagenes is only detected following growth at low temperatures (26°C) and in high concentrations of sodium chloride (290 mM) in the medium. The YsrSTR phosphorelay (PR) system is required forysaexpression and likely responds to NaCl. During our investigations into the Ysr PR system, we discovered that genes YE3578 and YE3579 are remarkably similar toysrRandysrS, respectively, and are probably a consequence of a gene duplication event. The amino acid differences between YE3578 andysrRare primarily clustered into two short regions. The differences between YE3579 andysrSare nearly all located in the periplasmic sensing domain; the cytoplasmic domains are 98% identical. We investigated whether these paralogs were capable of activatingysagene expression. We found that the sensor paralog, named DygS, is capable of compensating for loss ofysrS, but the response regulator paralog, DygR, cannot complement aysrRgene deletion. In addition, YsrR, but not DygR, interacts with the histidine phosphorelay protein YsrT. Thus, DygS likely activatesysagene expression in response to a signal other than NaCl and provides an example of a phosphorelay system in which two sensor kinases feed into the same regulatory pathway.IMPORTANCEAll organisms need mechanisms to promote survival in changing environments. Prokaryotic phosphorelay systems are minimally comprised of a histidine kinase (HK) that senses an extracellular stimulus and a response regulator (RR) but can contain three or more proteins. Through gene duplication, a unique hybrid HK was created. We show that, while the hybrid appears to retain all of the phosphorelay functions, it responds to a different signal than the original. Both HKs transmit the signal to the same RR, which activates a promoter that transcribes a set of genes encoding a type III secretion system (T3SS) whose function is not yet evident. The significance of this work lies in finding that two HKs regulate this T3SS, highlighting its importance.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Stephan Wimmi ◽  
Alexander Balinovic ◽  
Hannah Jeckel ◽  
Lisa Selinger ◽  
Dimitrios Lampaki ◽  
...  

AbstractMany bacterial pathogens use a type III secretion system (T3SS) to manipulate host cells. Protein secretion by the T3SS injectisome is activated upon contact to any host cell, and it has been unclear how premature secretion is prevented during infection. Here we report that in the gastrointestinal pathogens Yersinia enterocolitica and Shigella flexneri, cytosolic injectisome components are temporarily released from the proximal interface of the injectisome at low external pH, preventing protein secretion in acidic environments, such as the stomach. We show that in Yersinia enterocolitica, low external pH is detected in the periplasm and leads to a partial dissociation of the inner membrane injectisome component SctD, which in turn causes the dissociation of the cytosolic T3SS components. This effect is reversed upon restoration of neutral pH, allowing a fast activation of the T3SS at the native target regions within the host. These findings indicate that the cytosolic components form an adaptive regulatory interface, which regulates T3SS activity in response to environmental conditions.


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