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A small non‐coding RNA of the invasion gene island (SPI‐1) represses outer membrane protein synthesis from the Salmonella core genome
Author(s) -
Pfeiffer Verena,
Sittka Alexandra,
Tomer Raju,
Tedin Karsten,
Brinkmann Volker,
Vogel Jörg
Publication year - 2007
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2007.05991.x
Subject(s) - biology , pathogenicity island , gene , rna , salmonella , genetics , non coding rna , microbiology and biotechnology , genome , bacteria
Summary The Salmonella pathogenicity island (SPI‐1) encodes ∼35 proteins involved in assembly of a type III secretion system (T3SS) which endows Salmonella with the ability to invade eukaryotic cells. We have discovered a novel SPI‐1 gene, invR , which expresses an abundant small non‐coding RNA (sRNA). The invR gene, which we identified in a global search for new Salmonella s RNA genes, is activated by the major SPI‐1 transcription factor, HilD, under conditions that favour host cell invasion. The RNA chaperone, Hfq, is essential for the in vivo stability of the ∼80 nt InvR RNA. Hfq binds InvR with high affinity in vitro , and InvR co‐immunoprecipitates with FLAG epitope‐tagged Hfq in Salmonella extracts. Surprisingly, deletion/overexpression of invR revealed no phenotype in SPI‐1 regulation. In contrast, we find that InvR represses the synthesis of the abundant OmpD porin encoded by the Salmonella core genome. As invR is conserved in the early branching Salmonella bongori , we speculate that porin repression by InvR may have aided successful establishment of the SPI‐1 T3SS after horizontal acquisition in the Salmonella lineage. This study identifies the first regulatory RNA of an enterobacterial pathogenicity island, and new roles for Hfq and HilD in SPI‐1 gene expression.