Role of EnvC and the phosphoenolpyruvate:sugar phosphotransferase system in resistance to MreB disruption

Abstract

Cell wall synthesis in bacteria is determine by two protein complexes: the elongasome and divisome. The elongasome is coordinated by the actin homolog MreB while the divisome is organized by the tubulin homolog FtsZ. While these two systems must coordinate with each other to ensure that elongation and division are coregulated, this cross talk has been understudied. Using the MreB depolymerizing agent, A22, we found that multiple gene deletions result in cells exhibiting increased sensitivity to MreB depolymerization. One of those genes encodes for EnvC, a part of the divisome that is responsible for splitting daughter cells after the completion of cytokinesis through the activation of specific amidases. Here we show this increased sensitivity to A22 works through two known amidase targets of EnvC: AmiA and AmiB. In addition, suppressor analysis revealed that mutations in the phosphoenolpyruvate:sugar phosphotransferase system (PTS) can suppress the effects of A22 in both wild-type and envC deletion cells. Together this work helps to link elongation, division, and metabolism.

Disrupting central carbon metabolism increases antibiotic susceptibility inVibrio cholerae

“…(32). Interestingly, a recent study demonstrated that a ptsI mutation reduces the length of E. coli cells grown in LB broth, likewise suggesting a role for sugar uptake in cell division and/or elongation (39). These data seem to be in line with what we report here -both because they suggest that some glucose is available in LB broth, and because they imply a connection between sugar metabolism and cell envelope homeostasis and cell growth.…”