Drug-resistant K. pneumoniae poses a growing threat to public health, as carbapenem-resistant and hypervirulent lineages continue to drive high rates of treatment failure and mortality1,2,3. A deeper understanding of the molecular determinants that drive antimicrobial resistance is urgently needed, as it can directly inform the development of novel antibacterial agents and help improve the management and prognosis of patients with severe infections4. Establishing a direct link between a gene and resistance requires the construction of isogenic mutants that carry only the mutation of interest, removing the influence of unrelated background variation. Generating such precise mutants in K. pneumoniae has been challenging because widely accessible, reproducible genetic tools for point mutagenesis remain limited.
Conventional allelic-exchange methods that rely on suicide vectors and counterselection markers are often labor-intensive, require cloning of long homology arms, and produce low recombination frequencies in many clinical K. pneumoniae isolates5,6,7. The application of CRISPR/Cas9 genome editing has accelerated bacterial genetics by supplying a sequence-specific counterselection that strongly favors the recovery of edited cells8,9. The majority of published CRISPR/Cas9 approaches for Enterobacteriaceae, however, have been designed for gene inactivation or deletion and typically still demand assembly of new plasmids for each target, long repair templates, and multiple screening rounds10,11,12. Because many antimicrobial resistance phenotypes are caused by single-nucleotide substitutions in specific resistance genes, a dedicated point-mutation protocol is clearly needed. Here, the authors outline a streamlined procedure for installing precise, markerless point mutations in K. pneumoniae that relies exclusively on two accessible plasmids, pCasKP-apr and pSGKP-spe, originally developed for efficient editing in this species8. Notably, the two-plasmid system consisting of pCasKP-apr and pSGKP-spe has been successfully applied for gene inactivation and large-fragment deletion in K. pneumonia.
The method takes advantage of the strict PAM (3′-NGG) requirement of Cas9 protein, and the degeneracy of the genetic code—a short repair template is designed to carry the desired base change while also creating a synonymously mutated PAM sequence that is no longer recognized by Cas9. This dual modification is intended to prevent re-cleavage of the edited chromosome and to improve screening stringency. Under the conditions tested, this approach reduced the number of colonies that needed to be examined before the correct edit was found. By consolidating several steps, the protocol aims to make precise genome editing in K. pneumoniae more accessible to laboratories without specialized equipment, thereby facilitating genotype–phenotype analyses and supporting further study of AMR mechanisms.