SrcA contributes to Salmonella fitness in an animal host 
Most SsrB-regulated gene products contribute to the intracellular survival of Salmonella in a host.
In comparative genomics analyses, srcA was found in all virulent strains of Salmonella enterica containing SPI-2, but was absent from the cold-blooded animal commensal, S. bongori, which lacks SPI-2 (Table S1).
This suggested a co-evolution of srcA with the SPI-2 T3SS and a possible functional relationship.
If so, we reasoned that SrcA should contribute to animal colonization because the SPI-2 T3SS is essential for host infection.
To determine whether SrcA contributes to Salmonella fitness in a host, we created an unmarked in-frame srcA deletion in S.
Typhimurium and competed this strain against wild type cells in mixed oral infections of mice [25].
After three days of infection the geometric mean competitive index (CI) for the mutant was 0.20 (95%CI 0.13-0.29) and 0.18 (95%CI 0.06-0.5) in the spleen and liver respectively (P<0.0001; Fig. 1D) indicating that bacteria lacking srcA were significantly out competed by wild type cells during systemic infection.
To verify the role of srcA on this phenotype, we complemented the srcA mutant with a wild type srcA gene under the control of its endogenous promoter, which restored in vivo fitness to that of wild type (Fig. 1D).
The level of attenuation of the srcA mutant was generally higher than most single effector gene mutants [26], which suggested to us that SrcA contributes to an important aspect of T3SS function in vivo.
