Fabienne Benz, Sarah Camara-Wilpert, Jakob Russel, Katharina G Wandera, Rimvydė Čepaitė, Manuel Ares-Arroyo, José Vicente Gomes-Filho, Frank Englert, Johannes A Kuehn, Silvana Gloor, Mario Rodríguez Mestre, Aline Cuénod, Mònica Aguilà-Sans, Lorrie Maccario, Adrian Egli, Lennart Randau, Patrick Pausch, Eduardo P C Rocha, Chase L Beisel, Jonas Stenløkke Madsen, David Bikard, Alex R Hall, Søren Johannes Sørensen, Rafael Pinilla-Redondo
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...
May 7, 2024: Cell Host & Microbe