Disease relevance of msbA

• We now show that newly synthesized lipid A accumulates on the cytoplasmic side of the inner membrane after shifting an E. coli msbA missense mutant to the non-permissive temperature [1].
• Here, we have reported the construction and the characterization of a Neisseria meningitidis msbA mutant [2].

High impact information on msbA

• E. coli strains in which msbA synthesis is selectively shut off at 42 degreesC accumulate hexa-acylated lipid A and glycerophospholipids in their inner membranes [3].
• The msbA gene was originally discovered because when cloned on a low-copy-number plasmid vector it was able to suppress the temperature-sensitive growth phenotype of an htrB null mutant as well as the accumulation of phospholipids [4].
• The msbA gene is essential for bacterial viability at all temperatures [4].
• Translocation of the precursor to the outer membrane is restored by transformation with a plasmid containing the wild-type msbA gene [4].
• We report the characterization of the msbA gene, isolated as a multicopy suppressor of the HtrB temperature-sensitive phenotype [5].

Biological context of msbA

• Mutational analysis of msbA indicates that it may form an operon with a downstream gene, orfE, and that both of these genes are essential for bacterial viability under all growth conditions tested [5].

References