Draft genome sequence of a non-typeable USA300 isolate causing complicated bacteremia.

Spa-typing is a major genetic tool used to distinguish between strains. Interestingly, although rare, ~1%-2 of isolates are considered Spa-non-typeable . Herein, we present the draft genome sequence of just such a strain, TGH1097, a USA300 isolate from a complex bacteremia infection.

SSR42 is a Novel Regulator of Cytolytic Activity in .

Unlabelled: SSR42 is the longest noncoding RNA in the cell and the second-most abundant transcript in the stationary phase transcriptome, second only to RNAIII. It is highly conserved across strains and exhibits pronounced stability in stationary phase, however the mechanism behind its regulatory role has yet to be fully elucidated. Herein, we used transcriptomic and proteomic approaches to probe the role of SSR42, revealing that it is a powerful, novel activator of the primary leukocidin LukAB.

Coordinated adaptation of to calprotectin-dependent metal sequestration.

Unlabelled: The host protein calprotectin inhibits the growth of a variety of bacterial pathogens through metal sequestration in a process known as "nutritional immunity." growth is inhibited by calprotectin , and calprotectin is localized to staphylococcal abscesses during infection. However, the staphylococcal adaptations that provide defense against nutritional immunity and the role of metal-responsive regulators are not fully characterized.

Draft genome sequence of a highly proteolytic USA300 isolate from human urine.

The secreted proteases of have been shown to be critical during infection. Here, we present the draft genome sequence of TGH337, a hyper-proteolytic USA300 strain isolated from human urine.

Staphylococcus aureus SigS Induces Expression of a Regulatory Protein Pair That Modulates Its mRNA Stability.

SigS is the sole extracytoplasmic function sigma factor in Staphylococcus aureus and is necessary for virulence, immune evasion, and adaptation to toxic chemicals and environmental stressors. Despite the contribution of SigS to a myriad of critical phenotypes, the downstream effectors of SigS-dependent pathogenesis, immune evasion, and stress adaptation remain elusive. To address this knowledge gap, we analyzed the S.