Novel Effector Protein EspY3 of Type III Secretion System from Enterohemorrhagic Escherichia coli Is Localized in Actin Pedestals

Mariano Larzábal,Nahuel Riviere,Wanderson Marques Da Silva,Ángel Cataldi

doi:10.3390/microorganisms6040112

Mariano Larzábal, Nahuel Riviere + Show 2 more

Open Access

https://doi.org/10.3390/microorganisms6040112

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Journal: Microorganisms	Publication Date: Oct 27, 2018
Citations: 10	License type: CC BY 4.0

Affiliation: National Agricultural Technology Institute

Abstract

Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic Escherichia coli (EPEC) are attaching and effacing (A/E) pathogens, which translocate effector proteins to intestinal enterocytes through a type III secretion system (T3SS). T3SS and most of its effector proteins are encoded in a pathogenicity island called LEE. Recently, new effectors have been located outside the LEE. This study aimed to characterize EspY3, a novel non-LEE encoded T3SS effector of EHEC. EspY3 shares homology with SopD and PipB2 effector proteins of Salmonella’s T3SS-1 and T3SS-2, respectively. The presence of recombinant EspY3 in the supernatant samples demonstrated that EspY3 was secreted by the T3SS of EHEC and EPEC. Through infection assays, we demonstrated the translocation of EspY3 into Caco-2 cells by T3SS of EPEC. The subcellular localization of EspY3 was determined in the pedestal region, where its presence generates a significant increase in the size of the pedestals area. The EspY3 effector induced the elongation of polymerized actin pedestals in infected Caco-2 by EPEC. This study confirmed that EspY3 is part of the repertoire of T3SS effectors of EHEC O157:H7, and that it participates in modeling cellular actin during the infection.

Highlights

Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic Escherichia coli (EPEC) are an important cause of food and water-borne illnesses in humans worldwide
We have demonstrated that EspY3 is secreted into the environment in a T3SS-dependent manner in EHEC O157:H7
Many reports indicate that substrates of T3SS are recognized by the similar mechanism of another pathogen, for example, YopE effector protein of Yersinia can be secreted by T3SS of Salmonella [28]

Summary

Introduction

Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic Escherichia coli (EPEC) are an important cause of food and water-borne illnesses in humans worldwide. The formation of the attaching and effacing lesion involves the intimate attachment of the bacteria to the hosts intestinal epithelial cells, the effacement of intestinal microvilli, and the formation of actin-filled protrusions or “pedestals” [4]. The ability of these pathogens to generate the A/E lesion is given by the type III secretion system (T3SS), which is encoded in the pathogenicity island called locus of enterocyte effacement (LEE) [5]. One of the most representative effectors of EPEC and EHEC is Tir (translocated intimin receptor), which is encoded inside the LEE. LEE-encoded effectors of EHEC and EPEC are sufficient to cause the A/E lesion

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