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

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Benz, Fabienne | Camara-Wilpert, Sarah | Russel, Jakob | Wandera, Katharina | Čepaitė, Rimvydė | Ares-Arroyo, Manuel | Gomes-Filho, José Vicente | Englert, Frank | Kuehn, Johannes | Gloor, Silvana | Mestre, Mario Rodríguez | Cuénod, Aline | Aguilà-Sans, Mònica | Maccario, Lorrie | Egli, Adrian | Randau, Lennart | Pausch, Patrick | Rocha, Eduardo, P. C. | Beisel, Chase | Madsen, Jonas Stenløkke | Bikard, David | Hall, Alex | Sørensen, Søren Johannes | Pinilla-Redondo, Rafael

Edité par CCSD -

International audience. 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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