In the previous movie FtsZ (yellow) gets displaced from FtsA (unlabeled) upon addition of the wt N-terminal peptide of PBP1b (magenta), but not the R6E point mutant 👇 (10/12)

To our surprise the peptide of PBP1b was predicted to interact with the same residue on FtsA than FtsZ. This may suggest a competitive binding for FtsZ and PBP1b to FtsA. Thanks to Roman Hajdu in @nartimsoole.bsky.social lab, we find evidence for this in supported lipid bilayer assays 🧪🔬 (9/12)

This lysis phenotype is specific for cells undergoing division. When inhibiting divisome formation with SulA expression, cells lacking PBP1b lyse significantly less, and when they do, they display smaller lesions which are likely attributed to the impaired side wall repair 🛠️ (6/12)

Having such compromised septa leads to catastrophic lysis events under osmotically stressed conditions originating from the division site (green = released DNA) 🌊🔬(5/12)