Open AccessEnvelope stress responses defend against type six secretion system attacks independently of immunity proteins
Author(s) -
Steven J. Hersch,
Nobuhiko Watanabe,
María Silvina Stietz,
Kevin Manera,
Fatima Kamal,
Brianne J. Burkinshaw,
Linh Lam,
Alexander Pun,
Meixin Li,
Alexei Savchenko,
Tao Dong
Publication year - 2020
Publication title -
nature microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.305
H-Index - 79
ISSN - 2058-5276
DOI - 10.1038/s41564-020-0672-6
Subject(s) - type vi secretion system , effector , biology , secretion , vibrio cholerae , microbiology and biotechnology , cell envelope , immunity , escherichia coli , immune system , virulence , gene , genetics , bacteria , biochemistry
The arms race among microorganisms is a key driver in the evolution of not only the weapons but also defence mechanisms. Many Gram-negative bacteria use the type six secretion system (T6SS) to deliver toxic effectors directly into neighbouring cells. Defence against effectors requires cognate immunity proteins. However, here we show immunity-independent protection mediated by envelope stress responses in Escherichia coli and Vibrio cholerae against a V. cholerae T6SS effector, TseH. We demonstrate that TseH is a PAAR-dependent species-specific effector highly potent against Aeromonas species but not against its V. cholerae immunity mutant or E. coli. A structural analysis reveals TseH is probably a NlpC/P60-family cysteine endopeptidase. We determine that two envelope stress-response pathways, Rcs and BaeSR, protect E. coli from TseH toxicity by mechanisms including capsule synthesis. The two-component system WigKR (VxrAB) is critical for protecting V. cholerae from its own T6SS despite expressing immunity genes. WigR also regulates T6SS expression, suggesting a dual role in attack and defence. This deepens our understanding of how bacteria survive T6SS attacks and suggests that defence against the T6SS represents a major selective pressure driving the evolution of species-specific effectors and protective mechanisms mediated by envelope stress responses and capsule synthesis.