Pathogenicity Islands

2018 ◽  
pp. 41-52
2020 ◽  
Vol 56 (9) ◽  
pp. 1055-1069
Author(s):  
N. I. Smirnova ◽  
A. A. Kritsky ◽  
J. V. Alkhova ◽  
E. Yu. Agafonova ◽  
E. Yu. Shchelkanova ◽  
...  

2007 ◽  
Vol 189 (15) ◽  
pp. 5608-5616 ◽  
Author(s):  
Elisa Maiques ◽  
Carles Úbeda ◽  
María Ángeles Tormo ◽  
María Desamparados Ferrer ◽  
Íñigo Lasa ◽  
...  

ABSTRACT SaPIbov2 is a member of the SaPI family of staphylococcal pathogenicity islands and is very closely related to SaPIbov1. Typically, certain temperate phages can induce excision and replication of one or more of these islands and can package them into special small phage-like particles commensurate with their genome sizes (referred to as the excision-replication-packaging [ERP] cycle). We have studied the phage-SaPI interaction in some depth using SaPIbov2, with special reference to the role of its integrase. We demonstrate here that SaPIbov2 can be induced to replicate by different staphylococcal phages. After replication, SaPIbov2 is efficiently encapsidated and transferred to recipient organisms, including different non-Staphylococcus aureus staphylococci, where it integrates at a SaPI-specific attachment site, attC , by means of a self-coded integrase (Int). Phages that cannot induce the SaPIbov2 ERP cycle can transfer the island by recA-dependent classical generalized transduction and can also transfer it by a novel mechanism that requires the expression of SaPIbov2 int in the recipient but not in the donor. It is suggested that this mechanism involves the encapsidation of standard transducing fragments containing the intact island followed by int-mediated excision, circularization, and integration in the recipient.


E. coli ◽  
2003 ◽  
pp. 99-112
Author(s):  
Tobias A. Oelschlaeger ◽  
Ulrich Dobrindt ◽  
Britta Janke ◽  
Barbara Middendorf ◽  
Helge Karch ◽  
...  

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Langgeng Agung Waskito ◽  
Muhammad Miftahussurur ◽  
Maria Inge Lusida ◽  
Ari Fahrial Syam ◽  
Rumiko Suzuki ◽  
...  

2018 ◽  
Vol 86 (5) ◽  
Author(s):  
Jikang Wu ◽  
Anice Sabag-Daigle ◽  
Mikayla A. Borton ◽  
Linnea F. M. Kop ◽  
Blake E. Szkoda ◽  
...  

ABSTRACT Salmonella enterica elicits intestinal inflammation to gain access to nutrients. One of these nutrients is fructose-asparagine (F-Asn). The availability of F-Asn to Salmonella during infection is dependent upon Salmonella pathogenicity islands 1 and 2, which in turn are required to provoke inflammation. Here, we determined that F-Asn is present in mouse chow at approximately 400 pmol/mg (dry weight). F-Asn is also present in the intestinal tract of germfree mice at 2,700 pmol/mg (dry weight) and in the intestinal tract of conventional mice at 9 to 28 pmol/mg. These findings suggest that the mouse intestinal microbiota consumes F-Asn. We utilized heavy-labeled precursors of F-Asn to monitor its formation in the intestine, in the presence or absence of inflammation, and none was observed. Finally, we determined that some members of the class Clostridia encode F-Asn utilization pathways and that they are eliminated from highly inflamed Salmonella -infected mice. Collectively, our studies identify the source of F-Asn as the diet and that Salmonella -mediated inflammation is required to eliminate competitors and allow the pathogen nearly exclusive access to this nutrient.


2004 ◽  
pp. 211-229
Author(s):  
Kate Unsworth ◽  
David Holden

Sign in / Sign up

Export Citation Format

Share Document