Regulated Control of the Assembly and Diversity of LPS by Noncoding sRNAs

Figure 1

Regulatory networks controlling the LPS biosynthesis and nonstoichiometric modifications of lipid A and the LPS core. The key role mediated by RpoE-regulated noncoding sRNAs MicA, RybB, and SlrA with their major targets and how RpoE responds to LPS defects is depicted. RNA polymerase in complex with RpoE also transcribes some of the lpt genes, whose products are involved in the LPS translocation. RybB plays the major role in controlling the LPS composition by the translational repression of WaaR in RpoE-inducing conditions. RpoE in turn is subjected to a negative feedback regulation by RybB and SlrA that downregulate the synthesis of major cell envelope components to achieve homeostasis. RpoE also transcribes the eptB gene leading to the modification of KdoII by P-EtN. The translation of eptB mRNA is repressed by PhoP/Q-regulated MgrR sRNA. MicA and GcvB by base-paring repress the phoP mRNA translation. MicA substrate also includes lpxT, whose product mediates phosphorylation of lipid A generating triphosphorylated lipid A. Central roles played by BasS/R-dependent lipid A modifications and PhoB/R-dependent GlcUA and P-EtN incorporation in regulating the core biosynthesis are indicated. On the right side, proteolytic regulation of the first committed step in the LPS biosynthesis mediated by the RpoH-dependent FtsH/LapB complex is presented. LapB also couples the LPS synthesis and assembly with translocation system. Translation repression of lpp by SlrA regulates the availability of fatty acid pools for the synthesis of phospholipids. Spot42 sRNA regulates the availability of sugar nucleotide precursors for glycosyltransferases in response to the presence of either galactose or glucose by inhibiting the translation of galK within the gal operon.