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[1]D. Bikard et al. “Programmable repression and activation of bacterial gene expression using an engineered CRISPR-Cas system”. In: Nucleic Acids Res. 41.15 (Aug. 2013), pp. 7429–7437.

[2]Florian Brandt et al. “The Native 3D Organization of Bacterial Polysomes”. In: Cell 136.2 (2009), pp. 261 –271. issn: 0092-8674. doi: http://dx.doi.org/10.1016/j.cell.2008.11.016.

[3]A. G. Cheng, D. Missiakas, and O. Schneewind. “The giant protein Ebh is a determinant of Staphylococcus aureus cell size and complement resistance”. In: J. Bacteriol. 196.5 (2014), pp. 971–981.

[4]A. L. Cheung, K. Nishina, and A. C. Manna. “SarA of Staphylococcus aureus binds to the sarA promoter to regulate gene expression”. In: J. Bacteriol. 190.6 (Mar. 2008), pp. 2239–2243.

[5]G. Domingue, J. W. Costerton, and M. R. Brown. “Bacterial doubling time modulates the effects of opsonisation and available iron upon interactions between Staphylococcus aureus and human neutrophils”. In: FEMS Immunol. Med. Microbiol. 16.3-4 (Dec. 1996), pp. 223–228.

[8]L. S. Qi et al. “Repurposing CRISPR as an RNA-guided platform for sequence-specific control of gene expression”. In: Cell 152.5 (Feb. 2013), pp. 1173–1183.