Ming Li

The paper shows Pseudomonas aeruginosa uses a CRISPR-Cas system to silence a proline-codon toxin that stops phage growth, revealing a defense mechanism against anti-CRISPR phages.

This study identifies a novel bacterial defense mechanism where nucleoid-associated proteins detect phage-induced genome damage by relocating to the cytoplasm and activating immune effectors.

The paper constructs a genome-wide CRISPRi library to identify acid tolerance genes in S. mutans and finds 95 associated genes involved in metabolism, tRNA modification, and transcriptional regulation.

This study shows CRISPR-Cas regulates diverse anti-phage systems via crlRNAs, balancing their expression to prevent autoimmunity and enhance anti-phage defense.

The paper identifies viral crlRNAs that suppress bacterial immunity by reprogramming Cas proteins and demonstrates their potential for mammalian genome editing.

This paper develops a compact type I-F2 CRISPR-Cas system for transcriptional activation and base editing in human cells, achieving a wide editing window and high efficiency.

The paper identifies a CRISPR-repressed toxin that provides population-level immunity against diverse anti-CRISPR elements by expelling them through abortive infection-like effects.

This study uses native CRISPR-Cas genome editing to analyze resistance mechanisms in a multidrug-resistant Pseudomonas aeruginosa strain, revealing synergistic effects between efflux pumps and target mutations.