Killing two birds with one stone: trans-kingdom suppression of PAMP/MAMP-induced immunity by T3E from enteropathogenic bacteria

Abstract

Within the past decade, remarkable similarities between the molecular organization of animal and plant systems for non-self discrimination were revealed. Obvious parallels exist between the molecular structures of the receptors mediating the recognition of pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs) with plant pattern recognition receptors strikingly resembling mammalian Toll-like receptors. Mitogen-activated protein kinase cascades, leading to the transcriptional activation of immunity-associated genes, illustrate the conservation of whole molecular building blocks of PAMP/MAMP-induced signaling. Enteropathogenic Salmonella and Escherichia coli use a type three secretion system (T3SS) to inject effector proteins into the mammalian host cell to subvert defense mechanisms and promote gut infection. Lately, disease occurrence was increasingly associated with bacteria-contaminated fruits and vegetables and common themes have emerged with regard to whether and how effectors target innate immune responses in a trans-kingdom manner. We propose that numerous Salmonella or E. coli effectors may be active in planta and tend to target central components (hubs) of immune signaling pathways.

Keywords: Escherichia coli; PAMP/MAMP; Salmonella; enteropathogenic bacteria; innate immunity; mammals; plants; type three effectors.

FIGURE 1

Overview of the PTI/MTI-suppressing function of type three effectors from enterobacteria and phytopathogenic bacteria. The perception of pathogen/microbe-associated molecular patterns (PAMPs/MAMPs) by pattern recognition receptors (PRRs) triggers signaling pathways conferring immunity (PTI/MTI) that are conserved in mammals and plants. Host-adapted bacterial pathogens use the type three secretion system (T3SS) to inject effectors (T3E) that compromise PTI/MTI. Components of basic plant defense and interfering pathogen effectors (black box) are depicted. See main text for additional details. Abbreviations used in the figure: TLR5, Toll-like receptor 5; FLS2, Flagellin Sensitive 2; MyD88, Myeloid Differentiation primary response gene 88; BAK1, BRI1-Associated receptor Kinase 1; BIK1, Botrytis-Induced Kinase 1; PBS1, AvrPphB susceptible 1; PBL, AvrPphB susceptible 1-like; IRAK1,4, Il-1 receptor associated kinase 1,4; TRAF6, TNF receptor associated factor 6; TAB1,2, TAK1 binding protein 1,2; TAK1, TGFβ activated Kinase 1; MEKKs, mitogen-activated protein kinase kinase kinases; MEKs/MKKs, mitogen-activated protein kinase kinases; MPKs, mitogen-activated protein kinases; JNK, c-Jun N-terminal kinase; p38, p38 mitogen-activated protein kinase; Erk, extracellular signal regulated kinase; IKKs, IkappaB kinases; IκB, inhibitor of kappa B; NF-κB, nuclear factor-kappa B; AP-1, activator protein 1; WRKY, WRKY transcription factor; MYB30, MYB domain protein 30.