Transcriptional regulation of host pathogen interactions from the point of view of Staphylococcus aureus Compared to other human pathogens S. aureus outstands with a remarkably broad spectrum of deseases: from minor skin infections over endocarditis pneumoniae and osteomyelitis to septic shock. The prerequisite is an arsenal of adaptation strategies encoded in the core and variable genome. It includes the coordinated expression of adhesins and toxins evasion of the immune system response to stress and starvation adaptation of the metabolism formation of biofilms and capsules antibiotic resistance and persistence on the skin in nasal epithelial cells and even in the inner of macrophages after phagocytosis. All these adaptation strategies enable S. aureus to colonize a diversity of niches within the human host. The inevitable requirement is the ability to activate the appropriate adaptation strategy at the right time and at the right place. S. aureus overcomes this challenge with a sophisticated regulatory network. This PhD thesis covers a broad spectrum of transcriptional regulators involved in S. aureus pathogenesis: (1) the quorum sensing system Agr (regulation of early and late stage virulence factors) (2) the Sar family (regulation of early and late stage virulence factors) (3) SaeRS (regulation of accessory exotoxins and adhesins) (4) CodY (response to amino acid starvation including extracellular proteases) (5) Sigma B (general stress response including virulence factors) (6) Rex (anaerobic energy metabolism) (7) CtsR and HrcA (protein quality ... Staphylococcus Transcriptomics Regulator CodY SarA Rex Interactions aureus Regulation Pathogen