d due to the different methods (CLIP-Seq., Ribosome Profiling) and bioinformatics analysis pipeline. In addition, we used virulence-optimized minimal media for our experimental setup, whereas Potts *et al*. used LB full media for bacterial growth. Also strain specific differences could influence the observed results of the different studies.

This study also documents that the Csr systems regulates the biosynthesis of aromatic amino acids, siderophores, and colanic acids in EPEC. As iron is usually limited and an essential trace element during infection, iron uptake is generally strongly linked with and essential for EPEC virulence^[@CR50]^. The influence of CsrA on the entire *ent* operon suggests that this regulator affects the expression of a transcription factor or the stability of the *entABCDEF* mRNA. The formation of a CsrA-*entC* mRNA complex by EMSAs (Fig. [S9](#MOESM1){ref-type="media"}) indicated that CsrA influence on the *ent* operon expression is direct. The effect of CsrA on enterochelin expression and on other siderophore biosynthesis pathways of *E. coli* has not been investigated in detail before. Nevertheless Potts *et al*. also observed an influence of CsrA on the iron metabolism in an enrichment analysis for the genes involved in enterobactin biosynthesis and iron transporters, which was not visible in the CLIP-seq analysis, and therefore probably an indirect effect of CsrA regulation^[@CR8]^. Anyhow the major regulator of iron homeostasis *fur* was not regulated in the study of Potts *et al*., consistent with our transcriptome analysis. In contrast, serval mRNA involved in iron storage (*ftnB*, *dps* and *bfr*)^[@CR8]^ were strongly repressed in the study of Potts *et al*., but not affected in our experimental setup. It is well known that iron metabolism is closely linked to the carbon metabolism of pathogens. For instance, expression of many virulence and metabolic genes are under control of the cAMP receptor protein CRP, a global regulator of genes for carbon source utilization in the ab