ArticleMicrobiologyOpen2013
Overexpression of the Escherichia coli TolQ protein leads to a null-FtsN-like division phenotype.
Article in MicrobiologyOpen, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- RNA-seq reveals multifaceted gene expression response to Fab production in Escherichia coli fed-batch processes with particular focus on ribosome stalling.Microbial cell factories · 2024Article
- The role of CenKR in the coordination ofmBio · 2023Article
- Recruitment of the TolA Protein to Cell Constriction Sites in Escherichia coli via Three Separate Mechanisms, and a Critical Role for FtsWI Activity in Recruitment of both TolA and TolQ.Journal of bacteriology · 2022Article
- Structural changes of bacterial nanocellulose pellicles induced by genetic modification of Komagataeibacter hansenii ATCC 23769.Applied microbiology and biotechnology · 2019Article
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Authors and funding
3 authors.
Funding
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Abstract
Mutations involving the Tol-Pal complex of Escherichia 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.
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