Cell division protein FtsK coordinates bacterial chromosome segregation and daughter cell separation in Staphylococcus aureus

Unregulated cell cycle progression may have lethal consequences and therefore, bacteria have various mechanisms in place for the precise spatiotemporal control of cell cycle events. We have uncovered a new link between chromosome replication/segregation and splitting of the division septum. We show that the DNA translocase domain-containing divisome protein FtsK regulates cellular levels of a peptidoglycan hydrolase Sle1, which is involved in cell separation in the bacterial pathogen Staphylococcus aureus. FtsK interacts with a chaperone (trigger factor, TF) and establishes a FtsK-dependent TF concentration gradient that is higher in the septal region. Trigger factor binds Sle1 and promotes its preferential export at the septal region, while also preventing Sle1 degradation by the ClpXP proteolytic machinery. Upon conditions that lead to paused septum synthesis, such as DNA damage or impaired DNA replication/segregation, TF gradient is dissipated and Sle1 levels are reduced, thus halting premature septum splitting.

Automated summary

Unregulated cell cycle progression in bacteria can have lethal consequences. A new study has revealed a link between chromosome replication/segregation and division septum splitting. The protein FtsK, which contains a DNA translocase domain, has been found to regulate the cellular levels of a peptidoglycan hydrolase Sle1. This regulation is crucial for cell separation in the bacterial pathogen Staphylococcus aureus.