Malcolm F. White

The paper defines the mechanism of the MANTIS defence system in Pseudomonas aeruginosa, showing how dual ATPases couple self-modification to non-self restriction through adenine hemimethylation and cleavage.

The paper describes a dimeric TIR effector, TSR1, that binds cA3 and degrades it to auto-limit its activity in type III CRISPR-mediated antiviral immunity.

This study investigates the structural and biochemical properties of Csx15, a ring nuclease that binds cyclic nucleotides and regulates antiviral defense by modulating cOA levels.

The paper shows the type II Panoptes system generates cyclic tri-adenylate (cA3) to keep a CARF-TM effector inactive, and its degradation leads to membrane permeabilization and growth arrest.

This study reports the first cultivation of an Asgard archaeal virus and describes its integration, excision, and replication, along with the host's unique antiviral defense systems.

This study describes the structure and mechanism of Crn4, a ring nuclease that degrades cyclic oligoadenylates and modulates type III CRISPR immunity.

The paper shows that a viral SAVED domain, AcrIII-2, degrades the CRISPR second messenger cA4, inhibiting its effectors.

The paper analyzes type III CRISPR-Cas loci across 38,742 prokaryotic genomes to identify and characterize ring nucleases that regulate cyclic oligoadenylate levels.

This study investigates the structure and function of a SAM-AMP lyase from Clostridium botulinum, showing its ability to substitute for a phosphodiesterase in providing anti-phage defence.

This paper develops a Cas10-based lateral flow assay for detecting 7SL-sRNA in cattle with active trypanosomiasis, showing high sensitivity and specificity during chronic infection phases.

This study investigates the role of NYN, a ribonuclease in the Bacteroides fragilis type III CRISPR system, showing it cleaves ssRNA in a Mn2+-dependent manner, likely involved in crRNA maturation for antiviral defence.

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.

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