ArticleFrontiers in microbiology2021
Disruption of the MreB Elongasome Is Overcome by Mutations in the Tricarboxylic Acid Cycle.
Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- The phosphoenolpyruvate phosphotransferase system regulates cell length and width through semi-independent pathways.Molecular biology of the cell · 2026Article
- Genetic basis of cefiderocol resistance inMicrobiology spectrum · 2026Article
- MreB: unraveling the molecular mechanisms of bacterial shape, division, and environmental adaptation.Cell communication and signaling : CCS · 2025Review
- Logical regulation of endogenous gene expression using programmable, multi-input processing CRISPR guide RNAs.Nucleic acids research · 2024Article
- Adaptation ofMicroorganisms · 2024Article
- Transcriptomic analyses of Vibrio parahaemolyticus under the phenyllactic acid stress.Applied microbiology and biotechnology · 2024Article
- Enzyme 1 of the phosphoenolpyruvate:sugar phosphotransferase system is involved in resistance to MreB disruption in wild-type and ∆envC cells.Molecular microbiology · 2022Article
- Nanotubes Formation inCells · 2022Article
- ZapG (YhcB/DUF1043), a novel cell division protein in gamma-proteobacteria linking the Z-ring to septal peptidoglycan synthesis.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The bacterial actin homolog, MreB, is highly conserved among rod-shaped bacteria and essential for growth under normal growth conditions. MreB directs the localization of cell wall synthesis and loss of MreB results in round cells and death. Using the MreB depolymerizing drug, A22, we show that changes to central metabolism through deletion of malate dehydrogenase from the tricarboxylic acid (TCA) cycle results in cells with an increased tolerance to A22. We hypothesize that deletion of malate dehydrogenase leads to the upregulation of gluconeogenesis resulting in an increase in cell wall precursors. Consistent with this idea, metabolite analysis revealed that malate dehydrogenase (mdh) deletion cells possess elevated levels of several glycolysis/gluconeogenesis compounds and the cell wall precursor, uridine diphosphate N-acetylglucosamine (UDP-NAG). In agreement with these results, the increased A22 resistance phenotype can be recapitulated through the addition of glucose to the media. Finally, we show that this increase in antibiotic tolerance is not specific to A22 but also applies to the cell wall-targeting antibiotic, mecillinam.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.