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Cell Rep. 2017 Aug 8;20(6):1278-1286. doi: 10.1016/j.celrep.2017.07.045.

Non-classical Protein Excretion Is Boosted by PSMα-Induced Cell Leakage.

Author information

1
Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine (IMIT), University of Tübingen, Auf der Morgenstelle 28, 72076 Tübingen, Germany.
2
Organismic Interactions, Interfaculty Institute of Microbiology and Infection Medicine (IMIT), University of Tübingen, Auf der Morgenstelle 28, 72076 Tübingen, Germany.
3
Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20814, USA.
4
Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine (IMIT), University of Tübingen, Auf der Morgenstelle 28, 72076 Tübingen, Germany. Electronic address: friedrich.goetz@uni-tuebingen.de.

Abstract

Release of cytoplasmic proteins into the supernatant occurs both in bacteria and eukaryotes. Because the underlying mechanism remains unclear, the excretion of cytoplasmic proteins (ECP) has been referred to as "non-classical protein secretion." We show that none of the known specific protein transport systems of Gram-positive bacteria are involved in ECP. However, the expression of the cationic and amphipathic α-type phenol-soluble modulins (PSMs), particularly of PSMα2, significantly increase ECP, while PSMβ peptides or δ-toxin have no effect on ECP. Because psm expression is strictly controlled by the accessory gene regulator (agr), ECP is also reduced in agr-negative mutants. PSMα peptides damage the cytoplasmic membrane, as indicated by the release of not only CPs but also lipids, nucleic acids, and ATP. Thus, our results show that in Staphylococcus aureus, PSMα peptides non-specifically boost the translocation of CPs by their membrane-damaging activity.

KEYWORDS:

GAPDH; Staphylococcus aureus; aldolase; cytoplasmic proteins; enolase; membrane damage; non-classical protein secretion; phenol-soluble-modulins

PMID:
28793253
PMCID:
PMC6129975
DOI:
10.1016/j.celrep.2017.07.045
[Indexed for MEDLINE]
Free PMC Article

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