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

During Staphylococcus aureus infections, bacterial cells bifurcate into distinct, specialized cell types that localize physically in different colonization tissues to simultaneously generate different infection types.

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

MreB filaments bind, orient, and move along the direction of greatest membrane curvature, thus orienting the insertion of new glycan strands around the cell circumference in a manner that may help establish and maintain rod shape.

The binding site and potential mechanism of human SCARF1 for lipoprotein recognition are identified by combining the crystal structural determination of the N-terminal fragments and biochemical and cellular assays.

Imaging experiments and simulations reveal that the biophysical mechanism for force generation needed to engulf a forespore is based on coordinated cell wall synthesis and degradation.

D-alanylated lipoteichoic acids support Drosophila juvenile growth.

The transition of Staphylococcus aureus from commensalism to invasive disease, bacteraemia, is a complex balancing act offsetting offensive and defensive virulence strategies involving the Tca cell wall stress stimulon locus.

To avoid recognition by the immune system, bacteria use autolysins to trim fragments of peptidoglycans that are exposed on the bacterial cell wall.