3 years ago

Coordinated delivery and function of bacterial MARTX toxin effectors

Coordinated delivery and function of bacterial MARTX toxin effectors
Karla J. F. Satchell, Patrick J. Woida
Bacteria often coordinate virulence factors to fine-tune the host response during infection. These coordinated events can include toxins counteracting or amplifying effects of another toxin or though regulating the stability of virulence factors to remove their function once it is no longer needed. Multifunctional autoprocessing repeats-in toxin (MARTX) toxins are effector delivery toxins that form a pore into the plasma membrane of a eukaryotic cell to deliver multiple effector proteins into the cytosol of the target cell. The function of these proteins includes manipulating actin cytoskeletal dynamics, regulating signal transduction pathways, and inhibiting host secretory pathways. Investigations into the molecular mechanisms of these effector domains are providing insight into how the function of some effectors overlap and regulate one another during infection. Coordinated crosstalk of effector function suggests that MARTX toxins are not simply a sum of all their parts. Instead, modulation of cell function by effector domains may depend on which other effector domain are co-delivered. Future studies will elucidate how these effectors interact with each other to modulate the bacterial host interaction. MARTX toxins are delivery platforms that form pores in eukaryotic cell plasma membranes to simultaneously deliver multiple effector proteins into target cells. The function of these proteins includes manipulating actin cytoskeletal dynamics, regulating signal transduction pathways, and inhibiting host secretory pathways. Investigation of individual effector domains is providing insight into their molecular function. This work will further speculate how individual effector function to modulate signaling may be influenced in the holotoxin other co-delivered effectors. This article is protected by copyright. All rights reserved.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/mmi.13875

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