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Type III secretion of the Salmonella effector protein SopE is mediated via an N-terminal amino acid signal and not an mRNA sequence

Lookup NU author(s): Dr Michail Karavolos, Dr Jeong-Jin Lee, Dr Anjam Khan

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Abstract

Type III secretion systems (TTSS) are virulence-associated components of many gram-negative bacteria that translocate bacterial proteins directly from the bacterial cytoplasm into the host cell. The Salmonella translocated effector protein SopE has no consensus cleavable amino-terminal secretion sequence, and the mechanism leading to its secretion through the Salmonella pathogenicity island 1 (SPI-1) TTSS is still not fully understood. There is evidence from other bacteria which suggests that the TTSS signal may reside within the 5′ untranslated region (UTR) of the mRNA of secreted effectors. We investigated the role of the 5′ UTR in the SPI-1 TTSS-mediated secretion of SopE using promoter fusions and obtained data indicating that the mRNA sequence is not involved in the secretion process. To clarify the proteinaceous versus RNA nature of the signal, we constructed frameshift mutations in the amino-terminal region of SopE of Salmonella enterica serovar Typhimurium SL1344. Only constructs with the native amino acid sequence were secreted, highlighting the importance of the amino acid sequence versus the mRNA sequence for secretion. Additionally, we obtained frameshift mutation data suggesting that the first 15 amino acids are important for secretion of SopE independent of the presence of the chaperone binding site. These data shed light on the nature of the signal for SopE secretion and highlight the importance of the amino-terminal amino acids for correct targeting and secretion of SopE via the SPI-1-encoded TTSS during host cell invasion.


Publication metadata

Author(s): Karavolos MH, Wilson M, Henderson J, Lee JJ, Khan CMA

Publication type: Article

Publication status: Published

Journal: Journal of Bacteriology

Year: 2005

Volume: 187

Issue: 5

Pages: 1559-1567

Print publication date: 01/03/2005

ISSN (print): 0021-9193

ISSN (electronic): 1067-8832

Publisher: American Society for Microbiology

URL: .http:/dx.doi.org/10.1128/JB.187.5.1559-1567.2005

DOI: 10.1128/JB.187.5.1559-1567.2005

PubMed id: 15716426


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