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A phage DUF669 protein mediates post-cleavage DNA repair against host CRISPR immunity

Heng Zhu, Shengkun Dai, Hewen Deng, Shifeng Hou, Yuelong Li, Xin Tan, Ning Jia, Nan Li, Yingfei Ma

Revista con revisión por paresAfirmaciones fuertes, leer con cuidadoUso en el mundo real

En palabras de los autores

Phages have evolved various anti-CRISPR (Acr) proteins or RNA-based anti-CRISPR (Racr) to evade host CRISPR immunity by direct interference. However, whether other counter-CRISPR mechanisms exist remains unexplored. Here, we report a phage-encoded two-protein system, termed Healer, which neutralizes CRISPR immunity via a post-cleavage DNA repair mechanism. This phage replication-associated system comprises two proteins: Gp63 (a DUF669 domain-containing protein), and Gp64 (an AAA domain-containing protein). Mechanistic investigations elucidate that Gp63 acts as a rapid-response effector of CRISPR-induced DNA breaks. After Gp63 binds ssDNA, it promotes Gp64-mediated homologous recombination, which repairs CRISPR-generated phage DNA breaks and supports phage viability. Notably, co-expression of the Healer system with Cas9/Cas12 in E. coli, P. aeruginosa, and A. baumannii demonstrated high phage genome-editing efficiency. Collectively, our findings reveal an important anti-CRISPR complementary strategy, providing a promising tool for genome engineering. Using affinity purification-mass spectrometry, these authors identified the Healer system, a phage two-protein effector that repairs CRISPR-mediated DNA breaks via homologous recombination.

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Apareció: miércoles, 23 de septiembre. Nature Communications. Revista con revisión por pares.

DOI: 10.1038/s41467-026-77998-9