In section 2.6, the authors report that honokiol enhances FtsZ polymerization in vitro in a concentration-dependent manner (light scattering and TEM data), while simultaneously inhibiting GTPase activity. However, the paper also claims that Z-ring formation is disrupted in vivo, with mislocalized FtsZ aggregates. Given that increased polymerization is observed in vitro, but functional ring assembly is disrupted in vivo, can the authors clarify whether the enhanced polymerization observed in vitro corresponds to physiologically relevant or aberrant polymer forms? Could the observed polymer stabilization be an artifact of assay conditions (e.g., ionic strength, buffer composition) versus an actual mechanism of antibacterial action?
