Chromosome replication, cell growth, division and shape: a personal perspective

Zaritsky, Arieh; Woldringh, Conrad L.

doi:10.3389/fmicb.2015.00756

Cited by 27 publications

(37 citation statements)

References 120 publications

(165 reference statements)

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“…This study substantiates the coordinative relationships between DNA replication, nucleoid morphology, cell division and dimensions [9,10]. It demonstrates that blocking DNA replication transiently enhances divisions in the population, likely of cells that had completed chromosome duplication, before fully inhibiting further divisions.…”

Section: Dna Replication Enhances Cell Division In a Certain Proportisupporting

confidence: 76%

Transient enhanced cell division by blocking DNA synthesis in Escherichia coli

et al. 2020

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Duplication of the bacterial nucleoid is necessary for cell division hence specific arrest of DNA replication inhibits divisions culminating in filamentation, nucleoid dispersion and appearance of a-nucleated cells. It is demonstrated here that during the first 10 min however, Escherichia coli enhanced residual divisions: the proportion of constricted cells doubled (to 40%), nucleoids contracted and cells remodelled dimensions: length decreased and width increased. The preliminary data provides further support to the existence of temporal and spatial couplings between the nucleoid/replisome and the sacculus/divisome, and is consistent with the idea that bacillary bacteria modulate width during the division process exclusively.

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Section: Dna Replication Enhances Cell Division In a Certain Proportisupporting

confidence: 76%

Transient enhanced cell division by blocking DNA synthesis in Escherichia coli

et al. 2020

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“…A key question is how cells regulate their growth and timing of division to ensure that they do not get abnormally large (or small). This problem has ben referred to literature as size homeostasis and is a vigorous area of current experimental research in diverse organisms [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. We investigate if phenomenological models of cell size dynamics based on SHS can provide insights into the control mechanisms needed for size homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Conditions for Cell Size Homeostasis: A Stochastic Hybrid System Approach

Vargas-García

Soltani

Singh

2016

IEEE Life Sci. Lett.

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A ubiquitous feature of living cells is their growth over time followed by division into daughter cells. How isogenic cell populations maintain size homeostasis, i.e., a narrow distribution of cell size, is an intriguing fundamental problem. We model cell size using a stochastic hybrid system, where a cell grows exponentially in size (volume) over time and probabilistic division events are triggered at discrete time intervals. Moreover, whenever division events occur, size is randomly partitioned among daughter cells. We first consider a scenario, where a timer (i.e., cell-cycle clock) that measures the time since the last division event regulates both the cellular growth and division rates. Analysis reveals that such a timer-controlled system cannot achieve size homeostasis, in the sense that, the cell-to-cell size variation grows unboundedly with time. To explore biologically meaningful mechanisms for controlling size we consider two classes of regulation: a size-dependent growth rate and a size-dependent division rate. Our results show that these strategies can provide bounded intercellular variation in cell size, and exact mathematical conditions on the form of regulation needed for size homeostasis are derived. Different known forms of size control strategies, such as, the adder and the sizer are shown to be consistent with these results. Interestingly, for timer-based division mechanisms, the mean cell size depends on the noise in the cell-cycle duration but independent of errors incurred in partitioning of volume among daughter cells. In contrast, the mean cell size decreases with increasing partitioning errors for size-based division mechanisms. Finally, we discuss how organisms ranging from bacteria to mammalian cells have adopted different control approaches for maintaining size homeostasis.

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“…Unicellular organisms employ diverse control strategies to maintain size homeostasis i.e., to ensure that they do not become abnormally large (or small) [1][2][3][4][5]. It is well known that cells within an isoclonal population, which presumably follow identical size-control strategies, can exhibit significant intercellular differences in size [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Analysis of noise mechanisms in cell size control

Modi¹,

Vargas-García²,

Ghusinga³

et al. 2016

Preprint

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At the single-cell level, noise features in multiple ways through the inherent stochasticity of biomolecular processes, random partitioning of resources at division, and fluctuations in cellular growth rates. How these diverse noise mechanisms combine to drive variations in cell size within an isoclonal population is not well understood. To address this problem, we systematically investigate the contributions of different noise sources in well-known paradigms of cell-size control, such as the adder (division occurs after adding a fixed size from birth) and the sizer (division occurs upon reaching a size threshold). Analysis reveals that variance in cell size is most sensitive to errors in partitioning of volume among daughter cells, and not surprisingly, this process is well regulated among microbes. Moreover, depending on the dominant noise mechanism, different size control strategies (or a combination of them) provide efficient buffering of intercellular size variations. We further explore mixer models of size control, where a timer phase precedes/follows an adder, as has been proposed in Caulobacter crescentus. While mixing a timer with an adder can sometimes attenuate size variations, it invariably leads to higher-order moments growing unboundedly over time. This results in the cell size following a power-law distribution with an exponent that is inversely dependent on the noise in the timer phase. Consistent with theory, we find evidence of power-law statistics in the tail of C. crescentus cell-size distribution, but there is a huge discrepancy in the power-law exponent as estimated from data and theory. However, the discrepancy is removed after data reveals that the size added by individual newborns from birth to division itself exhibits power-law statistics. Taken together, this study provides key insights into the role of noise mechanisms in size homeostasis, and suggests an inextricable link between timer-based models of size control and heavy-tailed cell size distributions.

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Chromosome replication, cell growth, division and shape: a personal perspective

Cited by 27 publications

References 120 publications

Transient enhanced cell division by blocking DNA synthesis in Escherichia coli

Transient enhanced cell division by blocking DNA synthesis in Escherichia coli

Conditions for Cell Size Homeostasis: A Stochastic Hybrid System Approach

Analysis of noise mechanisms in cell size control

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