The OxyS and MicF sRNAs are integrated into the enterobacterial response to oxidative stress. OxyS, induced by the hydrogen peroxide-responsive OxyR, down-regulates fhlA mRNA (encoding for a transcription factor regulating formate metabolism), and indirectly represses rpoS expression. In addition, OxyS-mediated repression of nusG results in increased expression of kilR, encoded in the cryptic Rac prophage. KilR sequesters FtsZ, thereby leading to inhibition of cell division and growth arrest, which allows the cell to facilitate DNA damage repair. MicF contributes to increased bacterial resistance against antibiotics of different classes by repressing the major porin OmpF. Additional targets of MicF include lpxR mRNA (encoding an LPS-modification enzyme), as well as lrp mRNA (encoding a transcriptional regulator of amino acid metabolism and transport). Expression of MicF is positively controlled by the transcription factors OmpR, MarA, Rob and SoxS, with the latter being induced in the presence of superoxide.