Dissection of a cis-regulatory element (CRM) in its native chromosomal context using CRISPR/Cas9 editing and novel 'Active Genetics' reveals new features of CRM function and insights into how such regulatory elements change during evolution.
Conflicts between CRISPR-Cas systems and antibiotic resistance plasmids can be exploited to selectively eliminate antibiotic resistance from Enterococcus faecalis populations.
The DNA flanks on either side of an R-loop differ in stability, and CRISPR-Cas12 enzymes form double-strand breaks by targeting the more unstable flank with their single DNase active site.
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.
Through novel, cell-specific CRISPR tools to disrupt molecular clock genes, it was revealed that circadian rhythms are coordinated through a network, rather than by the clock of 'master regulatory' neurons.
Computer simulations reveal the potential and limitations of recently proposed CRISPR-based cell lineage recorders, and suggest how the recorders' design can be optimised to yield more accurate cell lineage trees.
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 guide RNA and donor DNA of the CRISPR/Cas system tolerate large chemical modifications and can be engineered for enhanced delivery and gene editing.
