L. A. Marraffini

The paper identifies a viral RNA that activates a bacterial immune system by binding to a cyclase, revealing a conserved mechanism for antiviral defense.

This study shows that the {Phi}AP1.1 phage uses an anti-CRISPR protein to temporarily disable CRISPR immunity, then integrates into the CRISPR locus to modulate immunity through spacer deletion and transfer.

This study investigates how EiCsm6 degrades its activator cA6 and uses structural and functional analyses to reveal activation and self-inactivation mechanisms of the CRISPR ribonuclease.

This study shows that type II CRISPR-Cas systems can generate spacer diversity at the cellular level, enabling survival of bacterial communities under phage infection on solid media.

The paper uses single-molecule fluorescence microscopy to study Cas10 dynamics in type III CRISPR-Cas systems, revealing conformational changes that distinguish self from nonself RNA.