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The bacterial lipoprotein modification enzyme Lgt is essential for viability and virulence. It catalyses the first committed step in the post-translational modification pathway by adding a diacylglyceryl moiety from membrane phospholipids onto preprolipoproteins. After complete maturation, lipoproteins fulfill various important functions in the bacterial cell envelope. We are particularly interested in Lgt as an antibiotic target to fight Gram-negative pathogenic bacteria. We showed that depletion of Lgt in H. pylori leads to growth arrest, reduction of viability and an aberrant cell morphology. Strikingly, cells are able to compensate for loss of Lgt following extended growth under depletion conditions. Our WGS sequencing data of these so-called revertants hint to regulation of gene expression, possibly through non-coding small RNAs, resulting in compensation of cell envelope processes leading to survival. In this project, the goal is to identify and characterize the transcriptome of the original mutant and its revertants to obtain detailed insight into the interconnectivity of cell envelope processes in H. pylori.
