FtsN maintains active septal cell wall synthesis by forming a processive complex with the septum-specific peptidoglycan synthases in E. coli.

FtsN plays an essential role in promoting the inward synthesis of septal peptidoglycan (sPG) by the FtsWI complex during bacterial cell division. How it achieves this role is unclear. Here we use single-molecule tracking to investigate FtsN's dynamics during sPG synthesis in E.

Comparative Study of Bacterial SPOR Domains Identifies Functionally Important Differences in Glycan Binding Affinity.

Bacterial SPOR domains target proteins to the divisome by binding septal peptidoglycan (PG) at sites where cell wall amidases have removed stem peptides. These PG structures are referred to as denuded glycans. Although all characterized SPOR domains bind denuded glycans, whether there are differences in affinity is not known.

Lysozyme Resistance in Clostridioides difficile Is Dependent on Two Peptidoglycan Deacetylases.

() is a major cause of hospital-acquired infections leading to antibiotic-associated diarrhea. exhibits a very high level of resistance to lysozyme. Bacteria commonly resist lysozyme through modification of the cell wall.

Glycerol Monolaurate (GML) and a Nonaqueous Five-Percent GML Gel Kill and Spores.

Glycerol monolaurate is a broadly antimicrobial fatty acid monoester, killing bacteria, fungi, and enveloped viruses. The compound kills stationary-phase cultures of , suggesting that the molecule may kill spores. In this study, we examined the ability of glycerol monolaurate alone or solubilized in a nonaqueous gel to kill vegetative cells and spores of aerobic , , and and anaerobic and () Glycerol monolaurate alone was bactericidal for all five organisms tested.

Multiple factors contribute to bimodal toxin gene expression in Clostridioides (Clostridium) difficile.

Clostridioides (formerly Clostridium) difficile produces two major toxins, TcdA and TcdB, upon entry into stationary phase. Transcription of tcdA and tcdB requires the specialized sigma factor, σ , which also directs RNA Polymerase to transcribe tcdR itself. We fused a gene for a red fluorescent protein to the tcdA promoter to study toxin gene expression at the level of individual C.