Blake Wiedenheft

The paper profiles RNA modifications in MS2 bacteriophage using LC-MS/MS and Nanopore DRS, finding {Psi} as the predominant modification.

The paper determines structures of the Cas1-2/3 complex to elucidate how it captures, delivers, and integrates foreign DNA into CRISPR loci.

The paper reveals a novel DNA homopolymer synthesis mechanism by DRT9, triggered by viral infection to induce abortive infection and population-level immunity.

The paper identifies AcrIE9 as an inhibitor of E. coli K12 Type IE CRISPR-Cas system through a census of anti-CRISPR proteins in Enterobacterales.

The paper identifies a prophage-encoded sRNA, svsR, that reduces lytic phage infection in AIEC by repressing maltodextrin transport genes, thereby limiting phage receptor expression.

This study shows that PNMA1 and PNMA4, derived from retrotransposons, are essential for reproductive capacity, as their absence leads to subfertility and hormonal changes in mice and associations with reproductive traits in humans.

The paper determines the structure of a type I-A retron and shows how it mediates antiphage defense through DNA degradation and nuclease activation.

The paper shows that viral proteins activate PARIS-mediated tRNA degradation, and viral tRNAs rescue infection by preventing cleavage.

The paper analyzes the evolutionary trajectories of domesticated metaviral capsid genes in mammals, revealing diverse outcomes and structural features of these genes.

This paper develops CRISPR-based RNA editing tools for precise deletions and insertions in RNA, enabling recombinant RNA virus engineering.

This paper demonstrates that CRISPR-guided RNA breaks are repaired in human cells, enabling programmable RNA editing to restore gene function.

The paper presents the cryo-EM structure of the type I-F CRISPR surveillance complex and shows a conformational change that exposes a nuclease recruitment helix homologous to an anti-CRISPR protein.