Article Dans Une Revue Cell Host & Microbe Année : 2024

Type IV-A3 CRISPR-Cas systems drive inter-plasmid conflicts by acquiring spacers in trans

David Bikard

Résumé

Plasmid-encoded type IV-A CRISPR-Cas systems lack an acquisition module, feature a DinG helicase instead of a nuclease, and form ribonucleoprotein complexes of unknown biological functions. Type IV-A3 systems are carried by conjugative plasmids that often harbor antibiotic-resistance genes and their CRISPR array contents suggest a role in mediating inter-plasmid conflicts, but this function remains unexplored. Here, we demonstrate that a plasmid-encoded type IV-A3 system co-opts the type I-E adaptation machinery from its host, Klebsiella pneumoniae (K. pneumoniae), to update its CRISPR array. Furthermore, we reveal that robust interference of conjugative plasmids and phages is elicited through CRISPR RNA-dependent transcriptional repression. By silencing plasmid core functions, type IV-A3 impacts the horizontal transfer and stability of targeted plasmids, supporting its role in plasmid competition. Our findings shed light on the mechanisms and ecological function of type IV-A3 systems and demonstrate their practical efficacy for countering antibiotic resistance in clinically relevant strains.
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pasteur-04785210 , version 1 (15-11-2024)

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Fabienne Benz, Sarah Camara-Wilpert, Jakob Russel, Katharina Wandera, Rimvydė Čepaitė, et al.. Type IV-A3 CRISPR-Cas systems drive inter-plasmid conflicts by acquiring spacers in trans. Cell Host & Microbe, 2024, 32 (6), pp.875-886.e9. ⟨10.1016/j.chom.2024.04.016⟩. ⟨pasteur-04785210⟩
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