Luciano A. Marraffini

Brig3, a DNA glycosylase from a soil metagenome, excises 5-hydroxymethylcytosine from T-even phage DNA; the glucose hydrolase BapA extends defense to glucosylated genomes such as wild-type T4.

This study identifies MtvS1 and MtvS2 as regulators of the Francisella type V-A CRISPR-Cas system and shows they interact with RNA polymerase to modulate gene expression.

The paper identifies a lipid-gated mechanism in CRISPR-Cas systems that uses membrane depolarization to block viral replication.

This study shows that Mre11-Rad50 enhances spacer acquisition in a haloarchaeal Type I-B CRISPR-Cas system, while Fen1 does not play a significant role.

This study identifies Chp as a CARF-HAD phosphatase effector that mediates immunity during the type III-A CRISPR-Cas response by inducing growth arrest and depleting ATP and IMP.

This study reveals how cyclic tetra-adenylate binds to Cap1, inducing conformational changes that open a membrane pore and cause depolarization during the type III CRISPR immune response.

This study identifies how bacterial TIR domains recognize viral capsids to initiate defense by forming complexes that trigger NAD+ depletion.

The paper uses deep mutational scanning to identify Cas1 and Cas2 variants that enhance spacer acquisition in CRISPR-Cas systems, improving immunity against phage infection.

This study shows that the Cas10 nuclease activity in type III-A CRISPR-Cas systems relieves host dormancy to enable spacer acquisition and retention, enhancing broad-spectrum immunity.

This paper shows that RNA polymerase can dislodge Cas9 from DNA breaks, improving genome editing and bacterial immunity by increasing mutagenesis and phage resistance.