Tag

Bacterial Immunity

All articles tagged with #bacterial immunity

Phage protein Gp0.4 hijacks FtsZ to unlock bacterial immunity via CapRelEbc
science3 months ago

Phage protein Gp0.4 hijacks FtsZ to unlock bacterial immunity via CapRelEbc

CapRelEbc, a fused toxin–antitoxin system in E. coli, is activated during T7 phage infection only when the phage protein Gp0.4 binds to monomeric FtsZ, forming a Gp0.4–FtsZ–CapRelEbc ternary complex. Gp0.4 inhibits FtsZ polymerization, blocking cell division, and this FtsZ–Gp0.4 complex relieves CapRelEbc auto-inhibition to enable its toxin activity, which pyrophosphorylates tRNAs and halts translation to restrict phage replication. Activation requires FtsZ; phage escape mutants map to Gp0.4 (or FtsZ interaction surfaces) that disrupt this activation. The study uses yeast two-hybrid, ITC, HDX-MS, in vitro translation, and AlphaFold modeling to support a tripartite activation mechanism, illustrating how host factors contribute to bacterial innate immunity.”,

Conserved protein complexes unite diverse nuclease–NTPase systems in bacterial anti-phage defense
science4 months ago

Conserved protein complexes unite diverse nuclease–NTPase systems in bacterial anti-phage defense

A Nature Microbiology study analyzes 16 nuclease–NTPase defense operons, revealing that multi-subunit protein complex formation is a shared feature that enables broad nucleic acid degradation to defend against phages. Some systems (e.g., Azaca) specifically target modified phage DNA, while others show degenerate, genome-spanning cleavage, illustrating conserved mechanistic principles amid diverse defense strategies. The work combines large-scale cell biology, biochemistry, and AlphaFold3 modeling to define the molecular features governing immunity, with sequencing data and reagents deposited in public repositories.

CARD–NLR–like immunity hub gates gene transfer agent release in Caulobacter crescentus
biology4 months ago

CARD–NLR–like immunity hub gates gene transfer agent release in Caulobacter crescentus

A CARD–NLR–like system named LypABC in Caulobacter crescentus coordinates GTA particle release by driving host cell lysis, while not being required for DNA packaging; its activity is tightly controlled by the repressor RogA and the regulator CdxB, which also represses GTA activators gafYZ, thereby coupling GTA activation to lysis. Misregulation of LypABC is highly toxic and triggers widespread ghost cell formation, highlighting how bacterial immune modules can be repurposed to promote horizontal gene transfer via GTAs.