Silencing by H-NS Potentiated the Evolution of Salmonella

• DOI: 10.1371/journal.ppat.1004500
• Publication Date: 2014-11-06T19:40:48Z
• Authors: Sabrina S. Ali; Jeremy Soo; Chitong Rao; Andrea S. Leung; David Hon-Man Ngai; Alexander W. Ensm...; William Wiley Nav...
• Keywords: Pathogenicity island; Loss function; Bacterial genome size

The bacterial H-NS protein silences expression from sequences with higher AT-content than the host genome and is believed to buffer fitness consequences associated foreign gene acquisition. Loss of results in severe growth defects Salmonella, but underlying reasons were unclear. An experimental evolution approach was employed determine which secondary mutations could compensate for loss Salmonella. Six independently derived S. Typhimurium hns mutant strains serially passaged 300 generations prior whole sequencing. Growth rates all lineages dramatically improved during course experiment. Each acquired missense encoding paralog StpA a poorly understood paralog, while 5 deletions genes Salmonella Pathogenicity Island-1 (SPI-1) Type 3 secretion system critical invoke inflammation. We further demonstrate that SPI-1 misregulation primary contributor decreased mutants. Three additional function PhoPQ virulence regulatory system. Similarly wild type did not acquire these mutations. stpA arose oligomerization domain generated proteins varying degrees. variants most able functionally substitute displayed altered DNA binding properties resembled those H-NS. These findings indicate central Salmonellae by buffering negative caused defining characteristic species.