Salmonella Typhimurium is a Gram-negative facultative pathogen
that causes a range of diseases, from mild gastroenteritis
to severe systemic infection in a variety of animal
hosts. S. Typhimurium regulates virulence gene expression
by a silencing mechanism using nucleoid-associated proteins
such as Histone-like Nucleoid Structuring protein (H-NS)
silencing. We hypothesize that the posttranslational modification,
specifically protein acetylation, of proteins in gene
silencing systems could affect the pathogenic gene expression
of S. Typhimurium. Therefore, we created acetylation-deficient
mutant by deleting two genes, pat and pta, which are
involved in the protein acetylation pathway. We observed
that the pat and pta deletion attenuates mouse virulence and
also decreases Salmonella’s replication within macrophages.
In addition, the Δpat Δpta strain showed a decreased expression
of the horizontally-acquired virulence genes, mgtC,
pagC, and ugtL, which are highly expressed in low Mg2+. The
decreased virulence gene expression is possibly due to higher
H-NS occupancy to those promoters because the pat and
pta deletion increases H-NS occupancy whereas the same
mutation decreases occupancy of RNA polymerase. Our results
suggest that Pat- and Pta-mediated protein acetylation
system promotes the expression of virulence genes by regulating
the binding affinity of H-NS in S. Typhimurium.