Septin binding restricts Shigella growth and triggers intracellular tolerance.

Septin binding to cytoplasmic Shigella polymerizes circumferential filaments that inhibit bacterial growth and triggers a danger-signal stress response.

• Why it matters: Intracellular bacteria must tolerate cell-autonomous immunity, but the antibacterial activity and sensing mechanisms of septin cages around autophagy-targeted pathogens were unclear.
• What they did: Using advanced microscopy and cell-free reconstitution, the study shows septins form circumferentially oriented filaments that inhibit growth; RNA-sequencing links septin binding to upregulated T3SS effectors and a stress response.
• The result: Septin-bound Shigella show hyperpolarized membranes without lethally damaged envelopes, and septin binding increases polymyxin B impact; OspC1 blocks septin recruitment and cspC protects membrane potential during infection.