%0 Journal Article
%T Functional dissection of translocon proteins of the Salmonella Pathogenicity Island 2-encoded type III secretion system
%A Stefanie U H£¿lzer
%A Michael Hensel
%J BMC Microbiology
%D 2010
%I BioMed Central
%R 10.1186/1471-2180-10-104
%X Here we investigated the structural requirements of SseB and SseD to form a functional translocon. Based on bioinformatic predictions, deletional analyses of SseB and SseD were performed and the effect on secretion by the T3SS, formation of a translocon, translocation of effector proteins and intracellular replication was investigated. Our data showed that both SseB and SseD are very sensitive towards alterations of the primary structure of the proteins. Although proteins encoded by mutant alleles were still secreted, we observed that all mutations resulted in a loss of function of the SPI2-T3SS.These observations indicate that translocon proteins of the SPI2-T3SS are highly evolved towards the formation of multi-subunit complex in the host cell membrane. Structural alterations are not tolerated and abrogate translocon function.Gram-negative bacteria have evolved various mechanisms for the transport of proteins across the bacterial envelope. Among these, type III secretion systems (T3SS) and type IV secretion systems are of specific interest since these systems mediate the vectorial transport of effector proteins into eukaryotic target cells [reviewed in [1]]. This process is termed translocation and requires the contact of the bacteria to a host cell membrane. T3SS are involved in a variety of bacteria-host cell interactions, ranging from symbiosis to pathogenesis [2]. Pathogenic bacteria deploy T3SS to translocate effector proteins with toxin-like activities and can manipulate various host cell functions by means of these effectors. Salmonella enterica is a facultative intracellular pathogen that has developed a unique intracellular lifestyle. Salmonella uses two distinct T3SS during different phases of pathogenesis [3]. The Salmonella Pathogenicity Island 1 (SPI1)-encoded T3SS mediates invasion of non-phagocytic cells and triggers inflammatory responses [reviewed in [3]].During the intracellular phase of pathogenesis, Salmonella resides within a specific organell
%U http://www.biomedcentral.com/1471-2180/10/104