Abstract
Salmonella effector protein SseJ is secreted by Salmonella into the host cell cytoplasm where it can then modify host cell processes. Whilst host cell small GTPase RhoA has previously been shown to activate the acyl-transferase activity of SseJ we show here an un-described effect of SseJ protein production upon microtubule dynamism. SseJ prevents microtubule collapse and this is independent of SseJ’s acyl-transferase activity. We speculate that the effects of SseJ on microtubules would be mediated via its known interactions with the small GTPases of the Rho family.
Highlights
Salmonellae are gram-negative bacteria that can infect a wide range of hosts and in humans can cause diseases such as typhoid fever and gastroenteritis
The T3SS encoded by Salmonella pathogenicity island-1 (SPI-1; T3SS-1) is mostly active when extracellular Salmonella come into contact with a host cell and allows effector proteins to be translocated directly into the cell cytoplasm and causes the bacteria to be actively phagocytosed
Another T3SS encoded by Salmonella pathogenicity island-2 (SPI-2; T3SS-2) enables the bacteria to multiply intracellularly in a Salmonella containing vacuole (SCV) by allowing further effector proteins to be translocated directly from the Salmonella into the host cell cytoplasm
Summary
Salmonellae are gram-negative bacteria that can infect a wide range of hosts and in humans can cause diseases such as typhoid fever and gastroenteritis. The T3SS encoded by Salmonella pathogenicity island-1 (SPI-1; T3SS-1) is mostly active when extracellular Salmonella come into contact with a host cell and allows effector proteins to be translocated directly into the cell cytoplasm and causes the bacteria to be actively phagocytosed. Another T3SS encoded by Salmonella pathogenicity island-2 (SPI-2; T3SS-2) enables the bacteria to multiply intracellularly in a Salmonella containing vacuole (SCV) by allowing further effector proteins to be translocated directly from the Salmonella (through the phagosomal membrane) into the host cell cytoplasm It is unclear precisely how Salmonella uses its multiple T3SS effector proteins to survive intracellularly but theories range from delaying fusion with the degradative organelle the lysosome [2], though the role of the T3SS in this process is contested [3], to preventing the delivery of lysosomal hydrolases to the Salmonella-containing phagosomal compartment by altering mannose 6-phosphate receptor trafficking [4]. A finite number of intracellular membrane trafficking and signalling events can be manipulated by a pathogen and successful intracellular pathogens are PLOS ONE | DOI:10.1371/journal.pone.0172588 February 24, 2017
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