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Abstract
The Sec pathway plays a prominent role in protein export and membrane insertion, including the secretion of major bacterial virulence determinants. The accessory Sec constituent SecDF has been proposed to contribute to protein export. Deletion of Staphylococcus aureus secDF has previously been shown to reduce resistance, to alter cell separation, and to change the expression of certain virulence factors. To analyse the impact of the secDF deletion in S. aureus on protein secretion, a quantitative secretome analysis was performed. Numerous Sec signal containing proteins involved in virulence were found to be decreased in the supernatant of the secDF mutant. However, two Sec-dependent hydrolases were increased in comparison to the wild type, suggesting additional indirect, regulatory effects to occur upon deletion of secDF. Adhesion, invasion, and cytotoxicity of the secDF mutant were reduced in human umbilical vein endothelial cells. Virulence was significantly reduced using a Galleria mellonella insect model. Altogether, SecDF is a promising therapeutic target for controlling S. aureus infections.
Highlights
The Gram-positive pathogen Staphylococcus aureus is one of the leading causes of nosocomial infections [1]
These virulence factors have to be exported across the cytoplasmic membrane to reach their destined location: the membrane, the cell wall or the extracellular space
The translocase consists of i) the heterotrimeric complex SecYEG, which forms a hydrophilic channel through the cytoplasmic membrane; ii) the motor protein SecA, an ATPase; and iii) the heterotrimeric complex SecDF-YajC
Summary
The Gram-positive pathogen Staphylococcus aureus is one of the leading causes of nosocomial infections [1]. The prevalence of methicillin-resistant S. aureus (MRSA) has been increasing in recent years This has resulted in an alarming rise of communityassociated (CA-) MRSA infections in immunocompetent individuals [2,3,4]. In addition to its adaptive response to antibiotics [5], the success of S. aureus is based upon its huge array of virulence factors [6] helping S. aureus to avoid host immunity These virulence factors have to be exported across the cytoplasmic membrane to reach their destined location: the membrane, the cell wall or the extracellular space. The translocase consists of i) the heterotrimeric complex SecYEG, which forms a hydrophilic channel through the cytoplasmic membrane; ii) the motor protein SecA, an ATPase; and iii) the heterotrimeric complex SecDF-YajC. Deletion of YajC only showed a weak phenotype and its exact function is still unknown [15,16]
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