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Cell cycle-dependent regulation of FtsZ in Escherichia coli in slow growth conditions.

ABSTRACT: FtsZ is the key regulator of bacterial cell division. It initiates division by forming a dynamic ring-like structure, the Z-ring, at the mid-cell. What triggers the formation of the Z-ring during the cell cycle is poorly understood. In Escherichia coli, the common view is that FtsZ concentration is constant throughout its doubling time and therefore regulation of assembly is controlled by some yet-to-be-identified protein-protein interactions. Using a newly developed functional, fluorescent FtsZ reporter, we performed a quantitative analysis of the FtsZ concentration throughout the cell cycle under slow growth conditions. In contrast to the common expectation, we show that FtsZ concentrations vary in a cell cycle-dependent manner, and that upregulation of FtsZ synthesis correlates with the formation of the Z-ring. The first half of the cell cycle shows an approximately fourfold upregulation of FtsZ synthesis, followed by its rapid degradation by ClpXP protease in the last 10% of the cell cycle. The initiation of rapid degradation coincides with the dissociation of FtsZ from the septum. Altogether, our data suggest that the Z-ring formation in slow growth conditions in E. coli is partially controlled by a regulatory sequence wherein upregulation of an essential cell cycle factor is followed by its degradation.

SUBMITTER: Mannik J

PROVIDER: S-EPMC6311098 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Cell cycle-dependent regulation of FtsZ in Escherichia coli in slow growth conditions.

Männik Jaana J Walker Bryant E BE Männik Jaan J

Molecular microbiology 20181029 6

FtsZ is the key regulator of bacterial cell division. It initiates division by forming a dynamic ring-like structure, the Z-ring, at the mid-cell. What triggers the formation of the Z-ring during the cell cycle is poorly understood. In Escherichia coli, the common view is that FtsZ concentration is constant throughout its doubling time and therefore regulation of assembly is controlled by some yet-to-be-identified protein-protein interactions. Using a newly developed functional, fluorescent FtsZ ...[more]

PMID: 30230648

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Project description:The bacterial lifestyle is plastic, requiring transcriptional, translational, and metabolic tailoring for survival. These dynamic cellular processes are energy intensive; therefore, flexible energetics is requisite for adaptive plasticity. An intricate network of complementary and supplementary pathways exists in bacterial energy metabolism. There are two main entry points for electrons in the aerobic electron transport system, NADH dehydrogenase (NDH) and succinate dehydrogenase (SDH), receiving electrons from NADH and succinate, respectively. Aerobic bacterial phyla have a non-proton-pumping NADH dehydrogenase, which is often the primary dehydrogenase under aerobiosis. Here, we report adaptive changes supporting growth restoration in an Escherichia coli strain lacking the primary dehydrogenase. Growth optimization is achieved by reducing the activity of succinate dehydrogenase, and thus we demonstrate a physiological discord between proton-pumping NADH dehydrogenase and succinate dehydrogenase in supporting growth. Beyond the fundamental understanding of the bioenergetic network, identifying this compensatory feature provides impetus to rational antimicrobial combinations for targeting the non-proton-pumping dehydrogenase. IMPORTANCE Energy generation pathways are a potential avenue for the development of novel antibiotics. However, bacteria possess remarkable resilience due to the compensatory pathways, which presents a challenge in this direction. NADH, the primary reducing equivalent, can transfer electrons to two distinct types of NADH dehydrogenases. Type I NADH dehydrogenase is an enzyme complex comprising multiple subunits and can generate proton motive force (PMF). Type II NADH dehydrogenase does not pump protons but plays a crucial role in maintaining the turnover of NAD+. To study the adaptive rewiring of energy metabolism, we evolved an Escherichia coli mutant lacking type II NADH dehydrogenase. We discovered that by modifying the flux through the tricarboxylic acid (TCA) cycle, E. coli could mitigate the growth impairment observed in the absence of type II NADH dehydrogenase. This research provides valuable insights into the intricate mechanisms employed by bacteria to compensate for disruptions in energy metabolism.

Dataset Information

Cell cycle-dependent regulation of FtsZ in Escherichia coli in slow growth conditions.

Publications

Cell cycle-dependent regulation of FtsZ in Escherichia coli in slow growth conditions.

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