Mutations in cell elongation genesmreB, mrdAandmrdBsuppress the shape defect of RodZ-deficient cells

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Abstract

RodZ interacts with MreB and both factors are required to maintain the rod shape ofEscherichia coli. The assembly of MreB into filaments regulates the subcellular arrangement of a group of enzymes that synthesizes the peptidoglycan (PG) layer. However, it is still unknown how polymerization of MreB determines the rod shape of bacterial cells. Regulatory factor(s) are likely to be involved in controlling the function and dynamics of MreB. We isolated suppressor mutations to partially recover the rod shape inrodZdeletion mutants and found that some of the suppressor mutations occurred inmreB. All of themreBmutations were in or in the vicinity of domain IA of MreB. ThosemreBmutations changed the property of MreB filamentsin vivo. In addition, suppressor mutations were found in the periplasmic regions in PBP2 and RodA, encoded bymrdAandmrdBgenes. Similar to MreB and RodZ, PBP2 and RodA are pivotal to the cell wall elongation process. Thus, we found that mutations in domain IA of MreB and in the periplasmic domain of PBP2 and RodA can restore growth and rod shape to ΔrodZcells, possibly by changing the requirements of MreB in the process.

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