During CRISPR adaptation, Cas4 forms a ternary complex with the Cas1-Cas2 spacer integration complex, an interaction that coordinates substrate hand-off following precise, PAM-dependent prespacer processing prior to integration.

The tetrameric structure of a casposase bound to DNA and its biochemical properties show how a transposase could have evolved to perform CRISPR-Cas spacer acquisition.

Cooperation between evolutionarily disparate CRISPR-Cas modules allows bacteria to counter mutational escape by viruses.

Linking the DNA repair template to the Cas9 ribonucleoprotein complex enhances homology-directed repair of the induced DNA double strand break.

Adenoviral CRISPR/Cas9 gene knockdown of mutant Col8a2 achieves structural and functional rescue of murine Fuchs’ endothelial corneal dystrophy, the first demonstration of post-mitotic CRISPR-based knockdown for phenotypic restoration.

The protein p53 negatively impacts the ability of a CRISPR screen to discriminate between essential and non-essential genes, hence, p53 status should be considered in these screens.

The inhibitory influence of nucleosomes on CRISPR-Cas9 is mitigated by nucleosomal DNA breathing and chromatin remodeling.

Three-dimensional structure of CRISPR Cas7-11 shed light on protein evolution and guide development of biotechnology for RNA manipulations in cells.

Divergent Cas9 enzymes direct site-specific single-stranded RNA cleavage, reducing infection by RNA phage in vivo and enabling programmable, PAM-independent repression of gene expression in bacteria.

Cloning-free 3Cs technology is developed for the generation of sequence-bias-free covalently closed circular synthesized (3Cs) CRISPR/Cas gRNA libraries that can interrogate the coding and noncoding human genome.