A new anti-CRISPR gene promotes the spread of drug-resistance plasmids in Klebsiella pneumoniae.
Chunyu JiangChengzhi YuShuyi SunJiajia LinMufeng CaiZhenquan WeiLingling FengJianhui LiYan ZhangKe DongXiaokui GuoJinhong QinYu ZhangPublished in: Nucleic acids research (2024)
The Klebsiella pneumoniae (K. pneumoniae, Kp) populations carrying both resistance-encoding and virulence-encoding mobile genetic elements (MGEs) significantly threaten global health. In this study, we identified a new anti-CRISPR gene (acrIE10) on a conjugative plasmid with self-target sequence in K. pneumoniae with type I-E* CRISPR-Cas system. AcrIE10 interacts with the Cas7* subunit of K. pneumoniae I-E* CRISPR-Cas system. The crystal structure of the AcrIE10-KpCas7* complex suggests that AcrIE10 suppresses the I-E* CRISPR-Cas by binding directly to Cas7 to prevent its hexamerization, thereby preventing the surveillance complex assembly and crRNA loading. Bioinformatic and functional analyses revealed that AcrIE10 is functionally widespread across diverse species. Our study reports a novel anti-CRISPR and highlights its potential role in spreading resistance and virulence among pathogens.
Keyphrases
- crispr cas
- genome editing
- klebsiella pneumoniae
- escherichia coli
- multidrug resistant
- genome wide
- global health
- pseudomonas aeruginosa
- public health
- staphylococcus aureus
- copy number
- antimicrobial resistance
- biofilm formation
- dna methylation
- gene expression
- gram negative
- cystic fibrosis
- transcription factor
- candida albicans
- amino acid