Thomas Keith Wood

The paper shows that the Hha/TomB type VII TA system in E. coli promotes phage infection by activating cryptic prophage lytic genes, contrary to the typical phage inhibition role of TAs.

This study shows Methanosarcina acetivorans can convert acetate to ethanol and methane, producing 40% ethanol from acetate, more than from methane or with a modified Mcr.

This study shows H-NS silences bacterial antiviral immunity by compacting chromatin, and its deletion enhances phage defense in E. coli.

This paper engineers methyl-coenzyme M reductase (Mcr) to enhance methane and carbon dioxide capture by identifying beneficial substitutions that improve biofilm growth and methane capture.

The paper enhances reverse methanogenesis by silencing the native Mcr gene in engineered archaea to boost methane conversion into ethanol and acetate.

The paper shows that cells with low ribosome content form persister cells 80-fold more frequently than average, indicating persister formation is inversely related to ribosome abundance.

The paper identifies PinR, a serine recombinase in E. coli, which inverts prophage DNA to block T2 phage infection by creating a protein that prevents phage receptor binding.

This study shows that the host environment, not biofilm growth, activates stress responses in Staphylococcus aureus and leads to ciprofloxacin tolerance at the single-cell level.

This study shows bacteria can survive phage infection through mutation or by forming persisters, which survive without mutation and retain wild-type phage sensitivity.

The paper shows toxin/antitoxin systems induce persister cells to inhibit phage, working with restriction-modification systems to inactivate phage DNA.

The paper uses single-cell analysis to show that the MqsR/MqsA TA system in E. coli protects against oxidative stress via the cryptic prophage protease LfgB, which degrades MqsA to activate stress response genes.

This study shows that CRISPR-Cas in E. coli is active and suppresses cryptic prophages through RNAi, preventing cell death and persister cell resuscitation.

The paper identifies BPOET as a compound that stimulates persister cell resuscitation in E. coli by activating RluD, which enhances ribosome activity.

This study shows that phages help bacteria recognize kin by forming demarcation lines between different strains.