An organelle-tethering mechanism couples flagellation to cell division in bacteria.

In some free-living and pathogenic bacteria, problems in the synthesis and assembly of early flagellar components can cause cell-division defects. However, the mechanism that couples cell division with the flagellar biogenesis has remained elusive. Herein, we discover the regulator MadA that controls transcription of flagellar and cell-division genes in Caulobacter crescentus. We demonstrate that MadA, a small soluble protein, binds the type III export component FlhA to promote activation of FliX, which in turn is required to license the conserved σ54-dependent transcriptional activator FlbD. While in the absence of MadA, FliX and FlbD activation is crippled, bypass mutations in FlhA restore flagellar biogenesis and cell division. Furthermore, we demonstrate that MadA safeguards the divisome stoichiometry to license cell division. We propose that MadA has a sentinel-type function that senses an early flagellar biogenesis event and, through cell-division control, ensures that a flagellated offspring emerges. • MadA links flagellar assembly to cell division in Caulobacter crescentus • MadA binds to the flagellar export component FlhA and activates the regulator FlbD • FlhA tethers the FlbD activator FliX and mutations in FlhA bypass MadA requirement • MadA licenses cell division by securing the stoichiometry of divisome components Siwach et al. describe a mechanism that couples flagellar biogenesis with cell division in bacteria. They demonstrate a role for the protein MadA both in fine-tuning flagellar assembly and in licensing cell division, suggesting a mechanism for ensuring the inheritance of flagella in nascent daughter cells. [ABSTRACT FROM AUTHOR]