CapRel Ebc Detects 3-Protein Complex to Block T7 Phage as FtsZ Partner Proves Essential
Updated
Updated · Nature.com · Jun 12
CapRel Ebc Detects 3-Protein Complex to Block T7 Phage as FtsZ Partner Proves Essential
1 articles · Updated · Nature.com · Jun 12
Summary
CapRel Ebc was shown to activate only when bound to a ternary complex with T7 phage protein Gp0.4 and host cell-division protein FtsZ, not to either protein alone.
10^5-fold protection against T7 in E. coli pointed researchers to the trigger, and five evolved escape phage populations all carried mutations in gene 0.4 encoding Gp0.4.
382 nM binding between Gp0.4 and monomeric FtsZ, plus 937 nM binding of CapRel Ebc to the Gp0.4-FtsZ complex, supported a 1:1:1 assembly that switches CapRel into an active state.
FtsZ proved necessary but not sufficient: an FtsZ suppressor mutant largely abolished defense, while other FtsZ inhibitors such as SulA and Kil peptides failed to activate CapRel Ebc.
The findings broaden bacterial immunity models beyond phage-only triggers, suggesting some defenses detect phage effectors together with the host proteins they disrupt—an echo of effector-triggered immunity in eukaryotes.
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Molecular Arms Race: Discovery of the CapRelEbc-FtsZ-Gp0.4 Complex Reveals New Bacterial Defense and Phage Counter-Defense Mechanisms
Overview
This report highlights a major breakthrough in understanding how bacteria defend themselves against phage attacks. When a phage infects a bacterium, the CapRelEbc toxin-antitoxin system is activated: the antitoxin CapRelB is degraded, releasing the toxin CapRelE. CapRelE then targets and inhibits FtsZ, a protein essential for bacterial cell division, effectively stopping the cell from dividing and limiting phage spread. However, the T7 phage counters this by producing the Gp0.4 protein, which binds to FtsZ and prevents CapRelE from working. This dynamic reveals a sophisticated molecular arms race between bacteria and phages.