First identification of the molecular determinants driving contact-dependent predation in Myxococcus..

A novel innate defense mechanism of cell lysis involves the coordinated oligomerization of a defensin by interaction with the membrane lipid, phosphatidylinositol 4,5-bisphosphate.

The absence of oxygen prompts Staphylococcus aureus cells to rupture resulting in increased formation of biofilms, which are the etiological agents of recurrent infections.

Selective removal of Wall Teichoic Acids from the envelope of Streptococcus pneumoniae prevents bacteriolysis and directs zonal cell wall synthesis.

Unlike other similar enzymes, the antimicrobial enzyme PlyC can interact with and translocate eukaryotic membranes, and then lyse and kill intracellular bacteria.

The death of bacterial kin cells releases a danger signal that activates a posttranscriptional response in surviving cells, resulting in the rapid elaboration of interbacterial competition factors.

Genetic and molecular analyses identify and characterize an evolutionary battle over lysis timing wherein a bacteriophage delays lysis through lysis inhibition while a defensive phage satellite accelerates lysis.

Penicillin induces bacterial cell lysis by altering cell surface polymer biogenesis to cause the misactivation of a cell wall degrading enzyme.

Structural and biochemical analysis of a protein called Ecp6, which is produced by a tomato fungus, reveals how the protein prevents plants from launching an immune response to the chitin in fungal cell walls.

Genetic analysis identifies an enzyme of the malaria parasite that is required to seal its host red blood cell membrane upon invasion, a key requirement of this important intracellular pathogen.