Who's Your DadA? d-Alanine Levels Regulate Bacterial Stiffness

A central question in mechanobiology is how cellular-scale structures are established and regulated. In bacteria, the cell envelope is essential for mechanical integrity, protecting against environmental stresses and bearing the load from high turgor pressures.A central question in mechanobiology is how cellular-scale structures are established and regulated. In bacteria, the cell envelope is essential for mechanical integrity, protecting against environmental stresses and bearing the load from high turgor pressures. Trivedi et al. (mBio 9:e01340-18, 2018, https://doi.org/10.1128/mBio.01340-18) screened a Pseudomonas aeruginosa transposon library and identified genes that influence cell stiffness by measuring cell growth while cells were embedded in an agarose gel. Their findings provide a broad knowledge base for how biochemical pathways regulate cellular mechanical properties in this pathogen. Dozens of genes across diverse functional categories were implicated, suggesting that cellular mechanics is a systems-level emergent property. Furthermore, changes in d-alanine levels in a dadA (d-alanine dehydrogenase) mutant resulted in decreases in the expression of cell wall enzymes, cross-linking density, and cell stiffness. These insights into the biochemical and mechanical roles of dadA highlight the importance of systems-level investigations into the physical properties of cells

Failsafe mechanisms couple division and DNA replication in bacteria.

The past 20 years have seen tremendous advances in our understanding of the mechanisms underlying bacterial cytokinesis, particularly the composition of the division machinery and the factors controlling its assembly [1]. At the same time, we understand very little about the relationship between cell division and other cell-cycle events in bacteria. Here we report that inhibiting division in Bacillus subtilis and Staphylococcus aureus quickly leads to an arrest in the initiation of new rounds of DNA replication, followed by a complete arrest in cell growth. Arrested cells are metabolically active but are unable to initiate new rounds of either DNA replication or division when shifted to permissive conditions. Inhibiting DNA replication results in entry into a similar quiescent state in which cells are unable to resume growth or division when returned to permissive conditions. Our data suggest the presence of two failsafe mechanisms: one linking division to the initiation of DNA replication and another linking the initiation of DNA replication to division. These findings contradict the prevailing view of the bacterial cell cycle as a series of coordinated but uncoupled events. Importantly, the terminal nature of the cell-cycle arrest validates the bacterial cell-cycle machinery as an effective target for antimicrobial development

Failsafe mechanisms couple division and DNA replication in bacteria.

The past 20 years have seen tremendous advances in our understanding of the mechanisms underlying bacterial cytokinesis, particularly the composition of the division machinery and the factors controlling its assembly [1]. At the same time, we understand very little about the relationship between cell division and other cell-cycle events in bacteria. Here we report that inhibiting division in Bacillus subtilis and Staphylococcus aureus quickly leads to an arrest in the initiation of new rounds of DNA replication, followed by a complete arrest in cell growth. Arrested cells are metabolically active but are unable to initiate new rounds of either DNA replication or division when shifted to permissive conditions. Inhibiting DNA replication results in entry into a similar quiescent state in which cells are unable to resume growth or division when returned to permissive conditions. Our data suggest the presence of two failsafe mechanisms: one linking division to the initiation of DNA replication and another linking the initiation of DNA replication to division. These findings contradict the prevailing view of the bacterial cell cycle as a series of coordinated but uncoupled events. Importantly, the terminal nature of the cell-cycle arrest validates the bacterial cell-cycle machinery as an effective target for antimicrobial development

Species-Independent Attraction to Biofilms through Electrical Signaling

Bacteria residing within biofilm communities can coordinate their behavior through cell-to-cell signaling. However, it remains unclear if these signals can also influence the behavior of distant cells that are not part of the community. Using a microfluidic approach, we find that potassium ion channel-mediated electrical signaling generated by a Bacillus subtilis biofilm can attract distant cells. Integration of experiments and mathematical modeling indicates that extracellular potassium emitted from the biofilm alters the membrane potential of distant cells, thereby directing their motility. This electrically mediated attraction appears to be a generic mechanism that enables cross-species interactions, as Pseudomonas aeruginosa cells also become attracted to the electrical signal released by the B. subtilis biofilm. Cells within a biofilm community can thus not only coordinate their own behavior but also influence the behavior of diverse bacteria at a distance through long-range electrical signaling. PAPERCLIP