The type III secretion system effector network hypothesis

doi:10.1016/j.tim.2021.10.007

The type III secretion system effector network hypothesis

2022-06-01

38

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AI

J

Julia Sanchez‐Garrido *

D

David Ruano‐Gallego *

DOI：10.1016/j.tim.2021.10.007

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Abstract

En 中文

Type Ill secretion system (T3SS) effectors are key virulence factors that underpin the infection strategy of many clinically important Gram-negative pathogens, including Salmonella enterica, Shigella spp., enteropathogenic and enterohemorrhagic Escherichia coli and their murine equivalent, Citrobacter rodentium. The cellular processes or proteins targeted by the effectors can be common to multiple pathogens or pathogen-specific. The main approach to understanding T3SS-mediated pathogenesis has been to determine the contribution of one effector at a time, with the aim of piecing together individual functions and unveiling infection mechanisms. However, in contrast to this prevailing approach, simultaneous deletion of multiple effectors revealed that they function as an interconnected network in vivo, uncovering effector codependency and context-dependent effector essentiality. This paradigm shift in T3SS biology is at the heart of this opinion article.

Keywords:

ENTEROPATHOGENIC ESCHERICHIA-COLI

CITROBACTER-RODENTIUM

SUPRAMOLECULAR STRUCTURE

BACTERIAL PATHOGEN

PROTEIN SECRETION

COLONIZATION

INFECTION

VIRULENCE

RECEPTOR

TARGETS

The type III secretion system effector network hypothesis

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