Robust Growth of Escherichia coli

Wang, Ping; Robert, Lydia; Pelletier, James F.; Dang, Wei; Taddéi, François; Wright, Andrew; Jun, Suckjoon

doi:10.1016/j.cub.2010.04.045

Cited by 908 publications

(1,284 citation statements)

References 26 publications

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“…In fact, transient associations are beneficial for buffering growth against fluctuations in enzyme abundance. At a PBP2 abundance of ∼100 enzymes per cell (21), one would expect 1/√N ∼ 10% fluctuations, yet growth rate remains consistent through cell division (24). In addition, transient association loosens the requirement for an MreB complex to spatially and temporally order the steps of cell wall synthesis.…”

Section: Discussionmentioning

confidence: 99%

A dynamically assembled cell wall synthesis machinery buffers cell growth

Lee

Tropini

Hsin

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Assembly of protein complexes is a key mechanism for achieving spatial and temporal coordination in processes involving many enzymes. Growth of rod-shaped bacteria is a well-studied example requiring such coordination; expansion of the cell wall is thought to involve coordination of the activity of synthetic enzymes with the cytoskeleton via a stable complex. Here, we use singlemolecule tracking to demonstrate that the bacterial actin homolog MreB and the essential cell wall enzyme PBP2 move on timescales orders of magnitude apart, with drastically different characteristic motions. Our observations suggest that PBP2 interacts with the rest of the synthesis machinery through a dynamic cycle of transient association. Consistent with this model, growth is robust to large fluctuations in PBP2 abundance. In contrast to stable complex formation, dynamic association of PBP2 is less dependent on the function of other components of the synthesis machinery, and buffers spatially distributed growth against fluctuations in pathway component concentrations and the presence of defective components. Dynamic association could generally represent an efficient strategy for spatiotemporal coordination of protein activities, especially when excess concentrations of system components are inhibitory to the overall process or deleterious to the cell.

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Section: Discussionmentioning

confidence: 99%

A dynamically assembled cell wall synthesis machinery buffers cell growth

Lee

Tropini

Hsin

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…If a cell divides symmetrically, then both daughter cells are expected to divide roughly at the same rate when environmental factors and cell population densities are kept constant. In a recent experiment where individual bacterial cell division events were monitored, it was shown that the time between cell divisions (or generation time) is a highly stochastic variable, even for clonal cells [1]. Furthermore, the generation time distribution is a non-monotonic functions of chronological cell age, a, defined as the time since its birth.…”

Section: Introductionmentioning

confidence: 99%

“…This behaviour is not restricted to prokaryotes, and is also true for eukaryotes. It is known that the probability for cell division depends both on age and on cell size [1,2]. For instance, for cells of the same size (mouse lymphoblasts L1210) the probability of division increases with cell age and for cells of the same age, the probability of division increases with cell size [2].…”

Section: Introductionmentioning

confidence: 99%

Age-dependent stochastic models for understanding population fluctuations in continuously cultured cells

Stukalin

Aifuwa

Kim

et al. 2013

J. R. Soc. Interface.

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For symmetrically dividing cells, large variations in the cell cycle time are typical, even among clonal cells. The consequence of this variation is important in stem cell differentiation, tissue and organ size control, and cancer development, where cell division rates ultimately determine the cell population. We explore the connection between cell cycle time variation and populationlevel fluctuations using simple stochastic models. We find that standard population models with constant division and death rates fail to predict the level of population fluctuation. Instead, variations in the cell division time contribute to population fluctuations. An age-dependent birth and death model allows us to compute the mean squared fluctuation or the population dispersion as a function of time. This dispersion grows exponentially with time, but scales with the population. We also find a relationship between the dispersion and the cell cycle time distribution for synchronized cell populations. The model can easily be generalized to study populations involving cell differentiation and competitive growth situations.

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“…Even in single-celled organisms in which cell division is seemingly morphologically symmetric, such as fission yeast or Escherichia coli, asymmetric partitioning of cellular contents can still occur and have a differential impact on the aging/death fate of the two offspring (4)(5)(6)(7)(8). Asymmetric cell division is also a general phenomenon in mammalian cells (e.g., during development or in mitotically active tissues), where cell division typically leads to two cells with distinct fates, often with different replicative potential.…”

mentioning

confidence: 99%

Systematic analysis of asymmetric partitioning of yeast proteome between mother and daughter cells reveals “aging factors” and mechanism of lifespan asymmetry

Yang

McCormick

Zheng

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Budding yeast divides asymmetrically, giving rise to a mother cell that progressively ages and a daughter cell with full lifespan. It is generally assumed that mother cells retain damaged, lifespan limiting materials ("aging factors") through asymmetric division. However, the identity of these aging factors and the mechanisms through which they limit lifespan remain poorly understood. Using a flow cytometry-based, high-throughput approach, we quantified the asymmetric partitioning of the yeast proteome between mother and daughter cells during cell division, discovering 74 mother-enriched and 60 daughterenriched proteins. While daughter-enriched proteins are biased toward those needed for bud construction and genome maintenance, mother-enriched proteins are biased towards those localized in the plasma membrane and vacuole. Deletion of 23 of the 74 motherenriched proteins leads to lifespan extension, a fraction that is about six times that of the genes picked randomly from the genome. Among these lifespan-extending genes, three are involved in endosomal sorting/endosome to vacuole transport, and three are nitrogen source transporters. Tracking the dynamic expression of specific mother-enriched proteins revealed that their concentration steadily increases in the mother cells as they age, but is kept relatively low in the daughter cells via asymmetric distribution. Our results suggest that some mother-enriched proteins may increase to a concentration that becomes deleterious and lifespan-limiting in aged cells, possibly by upsetting homeostasis or leading to aberrant signaling. Our study provides a comprehensive resource for analyzing asymmetric cell division and aging in yeast, which should also be valuable for understanding similar phenomena in other organisms.aging | asymmetric cell division | proteome C ellular aging and asymmetric cell division are intimately linked. In budding yeast, asymmetric cell division yields a mother cell and a daughter cell that are easily distinguishable under the microscope. Tracking the fate of the mother lineage led to the discovery that individual mother cells have a finite replicative lifespan, defined by the number of daughters a mother cell produced before senescence (1). It is known that although the mother cell ages with each division, their daughters retain the same full lifespan independent of the age of the mother at least until the last few mother cell divisions (2, 3). Thus, the asymmetry in cell division leads to asymmetry of aging.Even in single-celled organisms in which cell division is seemingly morphologically symmetric, such as fission yeast or Escherichia coli, asymmetric partitioning of cellular contents can still occur and have a differential impact on the aging/death fate of the two offspring (4-8). Asymmetric cell division is also a general phenomenon in mammalian cells (e.g., during development or in mitotically active tissues), where cell division typically leads to two cells with distinct fates, often with different replicative potential. It has been argued...

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Robust Growth of Escherichia coli

Cited by 908 publications

References 26 publications

A dynamically assembled cell wall synthesis machinery buffers cell growth

A dynamically assembled cell wall synthesis machinery buffers cell growth

Age-dependent stochastic models for understanding population fluctuations in continuously cultured cells

Systematic analysis of asymmetric partitioning of yeast proteome between mother and daughter cells reveals “aging factors” and mechanism of lifespan asymmetry

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