Abstract:
:The Salmonella pathogenicity island (SPI-1) encodes approximately 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 sRNA 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 approximately 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.
journal_name
Mol Microbioljournal_title
Molecular microbiologyauthors
Pfeiffer V,Sittka A,Tomer R,Tedin K,Brinkmann V,Vogel Jdoi
10.1111/j.1365-2958.2007.05991.xsubject
Has Abstractpub_date
2007-12-01 00:00:00pages
1174-91issue
5eissn
0950-382Xissn
1365-2958pii
MMI5991journal_volume
66pub_type
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