1. The bacterial tubulin FtsZ requires its intrinsically disordered linker to direct robust cell wall construction
- Author
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Amanda Miguel, Kerwyn Casey Huang, Elizabeth L. Meier, Samantha M. Desmarais, Kousik Sundararajan, and Erin D. Goley
- Subjects
Immunoblotting ,General Physics and Astronomy ,Cytokinetic ring ,macromolecular substances ,Peptidoglycan ,Article ,General Biochemistry, Genetics and Molecular Biology ,Polymerization ,Cell wall ,03 medical and health sciences ,chemistry.chemical_compound ,Bacterial Proteins ,Microscopy, Electron, Transmission ,Cell Wall ,Caulobacter crescentus ,FtsZ ,Cell Shape ,030304 developmental biology ,chemistry.chemical_classification ,Microscopy ,0303 health sciences ,Multidisciplinary ,biology ,030306 microbiology ,General Chemistry ,Metabolism ,3. Good health ,Cell biology ,Intrinsically Disordered Proteins ,Cytoskeletal Proteins ,Enzyme ,Tubulin ,chemistry ,biology.protein ,bacteria ,biological phenomena, cell phenomena, and immunity ,Linker ,Cell Division - Abstract
The bacterial GTPase FtsZ forms a cytokinetic ring at midcell, recruits the division machinery, and orchestrates membrane and peptidoglycan cell wall invagination. However, the mechanism for FtsZ regulation of peptidoglycan metabolism is unknown. The FtsZ GTPase domain is separated from its membrane-anchoring C-terminal conserved (CTC) peptide by a disordered C-terminal linker (CTL). Here, we investigate CTL function in Caulobacter crescentus. Strikingly, production of FtsZ lacking the CTL (ΔCTL) is lethal: cells become filamentous, form envelope bulges, and lyse, resembling treatment with β-lactam antibiotics. This phenotype is produced by FtsZ polymers bearing the CTC and a CTL shorter than 14 residues. Peptidoglycan synthesis still occurs downstream of ΔCTL, however cells expressing ΔCTL exhibit reduced peptidoglycan crosslinking and longer glycan strands than wildtype. Importantly, midcell proteins are still recruited to sites of ΔCTL assembly. We propose that FtsZ regulates peptidoglycan metabolism through a CTL-dependent mechanism that extends beyond simple protein recruitment.
- Published
- 2015
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