3 years ago

A naturally occurring deletion in FliE from Salmonella enterica serovar Dublin results in an aflagellate phenotype and defective proinflammatory properties.

Bruno D'Alessandro, Lucía Yim, José A Chabalgoity, Laura Betancor, Arací Martínez, Sebastián Sasías, Adriana Martínez-Sanguiné, Andrés Iriarte
Salmonella enterica serovar Dublin is adapted to cattle, but able to infect humans with high invasiveness. An acute inflammatory response at the intestine helps to prevent Salmonella dissemination to systemic sites. Flagella contribute to this response by providing motility and FliC-mediated signaling through pattern recognition receptors. In a previous work, we reported a high frequency (11 out of 25) of S Dublin isolates lacking flagella, in a collection obtained from humans and cattle. The aflagellate strains were impaired in their pro-inflammatory properties, in vitro and in vivo The aim of this work was to elucidate the underlying cause of absence of flagella in S Dublin isolates. We report here that class 3 flagellar genes are repressed in the human aflagellate isolates, due to an impaired secretion of FliA-anti-Sigma factor, FlgM. This phenotype is due to an in-frame 42-nucleotide-deletion in the fliE gene, which codes for a protein located in the flagellar basal body. The deletion is predicted to produce a protein lacking amino acids 18-31. The aflagellate phenotype was highly stable; revertants were only obtained when fliA was artificially over-expressed combined with several successive passages in motility agar. DNA sequence analysis revealed that motile revertants resulted from duplications of DNA sequences in fliE adjacent to the deleted region. These duplications produced a FliE protein of similar length to wild-type and demonstrate that amino acids 18-31 of FliE are not essential. The same deletion was detected in S Dublin isolates obtained from cattle, indicating that this mutation circulates in nature.

Publisher URL: http://doi.org/10.1128/IAI.00517-17

DOI: 10.1128/IAI.00517-17

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