Functional analysis of the EsaB component of the Staphylococcus aureus Type VII secretion system

M Guillermina Casabona; Grant Buchanan; Martin Zoltner; Catriona P Harkins; Matthew T G Holden; Tracy Palmer

doi:10.1099/mic.0.000580

Functional analysis of the EsaB component of the Staphylococcus aureus Type VII secretion system

M Guillermina Casabona, Grant Buchanan, Martin Zoltner, Catriona P Harkins, Matthew T G Holden, Tracy Palmer

Research output: Contribution to journal › Article › peer-review

Abstract

Type VII secretion systems (T7SS) are found in many bacteria and secrete proteins involved in virulence and bacterial competition. In Staphylococcus aureus the small ubiquitin-like EsaB protein has been previously implicated as having a regulatory role in the production of the EsxC substrate. Here we show that in the S. aureus RN6390 strain, EsaB does not genetically regulate production of any T7 substrates or components, but is indispensable for secretion activity. Consistent with EsaB being an essential component of the T7SS, loss of either EsaB or EssC are associated with upregulation of a common set of iron acquisition genes. However, a further subset of genes were dysregulated only in the absence of EsaB. Quantitative western blotting indicates that EsaB is present at very low levels in cells. Substitution of a highly conserved
threonine for alanine or arginine resulted in a loss of EsaB activity and destabilisation of the protein. Taken together our findings show that EsaB is essential for T7SS activity in RN6390.

Original language	English
Pages (from-to)	1851-1863
Number of pages	13
Journal	Microbiology
Volume	163
Issue number	12
Early online date	22 Nov 2017
DOIs	https://doi.org/10.1099/mic.0.000580
Publication status	Published - 1 Dec 2017

Keywords

Protein secretion
T7SS
Regulation
Staphylococcus aureus

Access to Document

10.1099/mic.0.000580Licence: CC BY

Holden_2017_Microbiology_EsaBcomponent_CC
© 2017 The Authors. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Final published version, 2.09 MBLicence: CC BY

Cite this

@article{b89e3004b1f743fc81ca6d8340174127,

title = "Functional analysis of the EsaB component of the Staphylococcus aureus Type VII secretion system",

abstract = "Type VII secretion systems (T7SS) are found in many bacteria and secrete proteins involved in virulence and bacterial competition. In Staphylococcus aureus the small ubiquitin-like EsaB protein has been previously implicated as having a regulatory role in the production of the EsxC substrate. Here we show that in the S. aureus RN6390 strain, EsaB does not genetically regulate production of any T7 substrates or components, but is indispensable for secretion activity. Consistent with EsaB being an essential component of the T7SS, loss of either EsaB or EssC are associated with upregulation of a common set of iron acquisition genes. However, a further subset of genes were dysregulated only in the absence of EsaB. Quantitative western blotting indicates that EsaB is present at very low levels in cells. Substitution of a highly conservedthreonine for alanine or arginine resulted in a loss of EsaB activity and destabilisation of the protein. Taken together our findings show that EsaB is essential for T7SS activity in RN6390.",

keywords = "Protein secretion, T7SS, Regulation, Staphylococcus aureus",

author = "Casabona, {M Guillermina} and Grant Buchanan and Martin Zoltner and Harkins, {Catriona P} and Holden, {Matthew T G} and Tracy Palmer",

note = "This study was supported by the Wellcome Trust (through Investigator Award 10183/Z/15/Z to TP and through Clinical PhD studentship support to CPH through grant 104241/z/14/z), the Biotechnology and Biological Sciences Research Council and the Medical Research Council (through grants BB/H007571/1 and MR/M011224/1, respectively).",

year = "2017",

month = dec,

day = "1",

doi = "10.1099/mic.0.000580",

language = "English",

volume = "163",

pages = "1851--1863",

journal = "Microbiology",

issn = "1350-0872",

publisher = "Microbiology Society",

number = "12",

}

TY - JOUR

T1 - Functional analysis of the EsaB component of the Staphylococcus aureus Type VII secretion system

AU - Casabona, M Guillermina

AU - Buchanan, Grant

AU - Zoltner, Martin

AU - Harkins, Catriona P

AU - Holden, Matthew T G

AU - Palmer, Tracy

N1 - This study was supported by the Wellcome Trust (through Investigator Award 10183/Z/15/Z to TP and through Clinical PhD studentship support to CPH through grant 104241/z/14/z), the Biotechnology and Biological Sciences Research Council and the Medical Research Council (through grants BB/H007571/1 and MR/M011224/1, respectively).

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Type VII secretion systems (T7SS) are found in many bacteria and secrete proteins involved in virulence and bacterial competition. In Staphylococcus aureus the small ubiquitin-like EsaB protein has been previously implicated as having a regulatory role in the production of the EsxC substrate. Here we show that in the S. aureus RN6390 strain, EsaB does not genetically regulate production of any T7 substrates or components, but is indispensable for secretion activity. Consistent with EsaB being an essential component of the T7SS, loss of either EsaB or EssC are associated with upregulation of a common set of iron acquisition genes. However, a further subset of genes were dysregulated only in the absence of EsaB. Quantitative western blotting indicates that EsaB is present at very low levels in cells. Substitution of a highly conservedthreonine for alanine or arginine resulted in a loss of EsaB activity and destabilisation of the protein. Taken together our findings show that EsaB is essential for T7SS activity in RN6390.

AB - Type VII secretion systems (T7SS) are found in many bacteria and secrete proteins involved in virulence and bacterial competition. In Staphylococcus aureus the small ubiquitin-like EsaB protein has been previously implicated as having a regulatory role in the production of the EsxC substrate. Here we show that in the S. aureus RN6390 strain, EsaB does not genetically regulate production of any T7 substrates or components, but is indispensable for secretion activity. Consistent with EsaB being an essential component of the T7SS, loss of either EsaB or EssC are associated with upregulation of a common set of iron acquisition genes. However, a further subset of genes were dysregulated only in the absence of EsaB. Quantitative western blotting indicates that EsaB is present at very low levels in cells. Substitution of a highly conservedthreonine for alanine or arginine resulted in a loss of EsaB activity and destabilisation of the protein. Taken together our findings show that EsaB is essential for T7SS activity in RN6390.

KW - Protein secretion

KW - T7SS

KW - Regulation

KW - Staphylococcus aureus

U2 - 10.1099/mic.0.000580

DO - 10.1099/mic.0.000580

M3 - Article

C2 - 29165232

SN - 1350-0872

VL - 163

SP - 1851

EP - 1863

JO - Microbiology

JF - Microbiology

IS - 12

ER -

Functional analysis of the EsaB component of the Staphylococcus aureus Type VII secretion system

Abstract

Keywords

Access to Document

Fingerprint

Cite this