Overexpression of the E scherichia coli TolQ protein leads to a null‐FtsN‐like division phenotype

Mutations involving the Tol‐Pal complex of E scherichia coli result in a subtle phenotype in which cells chain when grown under low‐salt conditions. Here, the nonpolar deletion of individual genes encoding the cytoplasmic membrane‐associated components of the complex (TolQ, TolR, TolA) produced a similar phenotype. Surprisingly, the overexpression of one of these proteins, TolQ, resulted in a much more overt phenotype in which cells occurred as elongated rods coupled in long chains when grown under normal salt conditions. Neither TolR nor TolA overexpression produced a phenotype, nor was the presence of either protein required for the TolQ‐dependent phenotype. Consistent with their native membrane topology, the amino‐terminal domain of TolQ specifically associated in vivo with the periplasmic domain of FtsN in a cytoplasm‐based two‐hybrid analysis. Further, the concomitant overexpression of FtsN rescued the TolQ‐dependent phenotype, suggesting a model wherein the overexpression of TolQ sequesters FtsN, depleting this essential protein from the divisome during Gram‐negative cell division. The role of the Tol‐Pal system in division is discussed.