Changes in lipopolysaccharide structure induce the sigma(E)-dependent response of Escherichia coli.

The envelope of Escherichia coli is composed of an asymmetric lipid bilayer containing lipopolysaccharide, phospholipid and outer membrane proteins (OMPs). Physical and chemical stresses impact on the integrity of the outer membrane envelope and trigger the sigma(E)-dependent response, whereby E. coli activates the expression of genes that increase its capacity for folding OMPs and synthesizing lipopolysaccharide (LPS). While it has already been appreciated that misfolded OMPs induce the sigma(E) response, a role for LPS in activating this pathway was hitherto unknown. Here we show that ammonium metavandate (NH4VO3) induces multiple changes in E. coli LPS structure and activates the sigma(E)-dependent response without altering OMP. One such NH4VO3-mediated LPS decoration, the CrcA/PagP-catalysed addition of palmitate to lipid A, appeared to be alone sufficient to activate transcription at sigma(E)-dependent promoters. Furthermore, reduced acylation of LPS, caused by htrB or msbB mutations, also resulted in a constitutive expression of the sigma(E) regulon above wild-type levels. Production of these aberrant outer membrane lipids did not noticeably affect the composition or the amount of OMPs. A model is proposed whereby structural intermediates of the LPS biosynthetic pathway or modified LPS molecules may function as signals that activate the sigma(E) response.

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