Complex transcriptional and post‐transcriptional regulation of an enzyme for lipopolysaccharide modification. Issue 1 (31st May 2013)

• Record Type: Journal Article
• Authors: Moon, Kyung; Six, David A.; Lee, Hyun‐Jung; Raetz, Christian R. H.; Gottesman, Susan
• Is Part Of: Molecular microbiology. Volume 89:Issue 1(2013)
• Page Start: 52
• Page End: 64
• Publication Date: 2013-05-31
• Subjects: Molecular microbiology -- Periodicals; 572.829
• DOI: 10.1111/mmi.12257
• Languages: English
• ISSNs: 0950-382X

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>The PhoQ/PhoP two‐component system activates many genes for lipopolysaccharide (LPS) modification when cells are grown at low Mg<sup>2+</sup> concentrations. An additional target of PhoQ and PhoP is MgrR, an Hfq‐dependent small RNA that negatively regulates expression of <italic>eptB</italic>, also encoding a protein that carries out LPS modification. Examination of LPS confirmed that MgrR effectively silences EptB; the phosphoethanolamine modification associated with EptB is found in Δ<italic>mgrR</italic>::kan but not <italic>mgrR</italic><sup>+</sup> cells. Sigma E has been reported to positively regulate <italic>eptB</italic>, although the <italic>eptB</italic> promoter does not have the expected Sigma E recognition motifs. The effects of Sigma E and deletion of <italic>mgrR</italic> on levels of <italic>eptB</italic> mRNA were independent, and the same 5′ end was found in both cases. <italic>In vitro</italic> transcription and the behaviour of transcriptional and translational fusions demonstrate that Sigma E acts directly at the level of transcription initiation for <italic>eptB</italic>, from the same start point as Sigma 70. The results suggest that when Sigma E is active, synthesis of <italic>eptB</italic> transcript outstrips MgrR‐dependent degradation; presumably the modification of LPS is important under these conditions. Adding to the complexity of <italic>eptB</italic> regulation is a second sRNA, ArcZ, which also directly and negatively regulates <italic>eptB</italic>.</p> </abstract>