Shiomi D, Toyoda A, Aizu T, Ejima F, Fujiyama A, Shini T, Kohara Y, Niki H.
Mutations in cell elongation genes mreB, mrdA and mrdB suppress the shape defect of RodZ-deficient cells.
RodZ interacts with MreB and both factors are required to maintain the rod shape of Escherichia 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 in rodZ deletion mutants and found that some of the suppressor mutations occurred in mreB. All of the mreB mutations were in or in the vicinity of domain IA of MreB. Those mreB mutations changed the property of MreB filaments in vivo. In addition, suppressor mutations were found in the periplasmic regions in PBP2 and RodA, encoded by mrdA and mrdB genes. 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 ΔrodZ cells, possibly by changing the requirements of MreB in the process.
Cytoskeletal Proteins / deficiency*
Cytoskeletal Proteins / genetics
Escherichia coli / cytology*
Escherichia coli / genetics
Escherichia coli / metabolism*
Escherichia coli Proteins / genetics*
Escherichia coli Proteins / metabolism
Gene Expression Regulation, Bacterial
Membrane Proteins / genetics*
Membrane Proteins / metabolism
Penicillin-Binding Proteins / genetics*
Penicillin-Binding Proteins / metabolism
BIOCHEMISTRY & MOLECULAR BIOLOGY
|Prokaryotes E. coli