M. F. White

CRISPR antiphage defence mediated by the cyclic nucleotide-binding membrane protein Csx23

This study identifies Csx23 as a CRISPR effector that uses cyclic nucleotide binding to mediate antiphage defence in Vibrio cholerae.

Reversible conjugation of a CBASS nucleotide cyclase regulates immune response to phage infection

The paper shows that the CBASS system in bacteria uses protein conjugation to regulate nucleotide cyclase activity, keeping it inactive until phage infection triggers its release.

Antiviral Type III CRISPR signalling via conjugation of ATP and AdoMet

This study identifies SAM-AMP as a novel second messenger in type III-B CRISPR systems, used for antiviral signaling by conjugating ATP to S-adenosyl methionine.

Repurposing the atypical Type I-G CRISPR system for bacterial genome engineering

This study repurposes the type I-G CRISPR system for bacterial genome engineering, showing that Cas3 helicase activity is not essential for immunity and that the system can improve homology-directed repair efficiency.

Structure and mechanism of the type I-G CRISPR effector

This study reports the structure and function of the type I-G CRISPR effector from Thioalkalivibrio sulfidiphilus, revealing key molecular details about its composition and mechanism.

Cyclic nucleotide-induced superhelical structure activates a bacterial TIR immune effector

The paper shows a bacterial TIR-SAVED effector forms a superhelical structure upon binding cyclic tri-adenylate, enabling NAD+ degradation as part of an anti-viral defense mechanism.

SAVED by a toxin: Structure and function of the CRISPR Lon protease.

The paper reports the crystal structure of CRISPR-Lon, a protein that activates by binding cA4 and cleaves CRISPR-T to release a nuclease-like fragment.

Specificity and sensitivity of an RNA targeting type III CRISPR complex coupled with a NucC endonuclease effector

This study characterizes the VmeCmr type III CRISPR system's RNA targeting specificity and sensitivity, demonstrating its potential as a highly specific and sensitive assay for SARS-CoV-2 RNA detection.

Tetramerisation of the CRISPR ring nuclease Csx3 facilitates cyclic oligoadenylate cleavage

The paper identifies Csx3 as a ring nuclease that degrades cyclic tetra-adenylate (cA4), revealing its role in removing cOA molecules after viral infection.

Fuse to defuse: a self-limiting ribonuclease-ring nuclease fusion for type III CRISPR defence

The paper describes a fusion protein combining a ribonuclease and a ring nuclease to regulate cOA signaling in type III CRISPR systems, ensuring a time-limited immune response.

The dynamic interplay of host and viral enzymes in type III CRISPR-mediated cyclic nucleotide signalling

The paper examines how host and viral enzymes regulate cyclic nucleotide levels and infection outcomes in type III CRISPR systems.

Structure and mechanism of a Type III CRISPR defence DNA nuclease activated by cyclic oligoadenylate

This paper describes the structure and mechanism of Can1, a cOA-activated CRISPR defence DNA nuclease, showing how cA4 binding activates its DNA nicking activity.

A viral ring nuclease anti-CRISPR subverts type III CRISPR immunity

This study identifies a viral anti-CRISPR enzyme that degrades cyclic tetra-adenylate, neutralizing type III CRISPR immunity in bacteria and archaea.

Cyclic oligoadenylate signalling mediates Mycobacterium tuberculosis CRISPR defence

This study shows that Mycobacterium tuberculosis uses a type III-A CRISPR system with a cyclic hexa-adenylate (cA6) signalling pathway and the Csm6 ribonuclease for immunity against mobile genetic elements, rather than DNA cleavage.

A type III CRISPR ancillary ribonuclease degrades its cyclic oligoadenylate activator

The paper identifies TTHB144 as a self-limiting CRISPR ribonuclease that degrades its cyclic oligoadenylate activator, providing a mechanism to terminate RNA degradation after viral infection.

Ring nucleases deactivate Type III CRISPR ribonucleases by degrading cyclic oligoadenylate

The paper identifies a Ring nuclease that degrades cyclic oligoadenylate (cOA) to deactivate Type III CRISPR ribonucleases and terminate the antiviral state.