Autorepressor Model for Control of DNA Replication

Sompayrac, Lauren; Maaløe, O.

doi:10.1038/newbio241133a0

Cited by 174 publications

(150 citation statements)

References 7 publications

Supporting

Mentioning

143

Contrasting

Order By: Relevance

“…The mechanism for the second transition could be as described previously (33) for the transition probability hypothesis. The mechanism for the first transition could be accurate monitoring of a critical size by a titration mechanism (7) which is, however, normally distributed between cells, or imprecise monitoring of a critical size or imprecise specifying of a critical size, as has been suggested previously (34) for bacteria. Experimental distinctions between these possibilities will await knowledge of the molecules involved.…”

Section: Discussionmentioning

confidence: 99%

Size control models of Saccharomyces cerevisiae cell proliferation.

Wheals¹

1982

Mol. Cell. Biol.

View full text Add to dashboard Cite

By using time-lapse photomicroscopy, the individual cycle times and sizes at bud emergence were measured for a population of Saccharomyces cerevisiae cells growing exponentially under balanced growth conditions in a specially constructed filming slide. There was extensive variability in both parameters for daughter and parent cells. The data on 162 pairs of siblings were analyzed for agreement with the predictions of the transition probability hypothesis and the critical-size hypothesis of yeast cell proliferation and also with a model incorporating both of these hypotheses in tandem. None of the models accounted for all of the experimental data, but two models did give good agreement to all of the data. The wobbly tandem model proposes that cells need to attain a critical size, which is very variable, enabling them to enter a start state from which they exit with firstorder kinetics. The sloppy size control model suggests that cells have an increasing probability per unit time of traversing start as they increase in size, reaching a high plateau value which is less than one. Both models predict that the kinetics of entry into the cell division sequence will strongly depend on variability in birth size and thus will be quite different for daughters and parents of the asymmetrically dividing yeast cells. Mechanisms underlying these models are discussed.

show abstract

Section: Discussionmentioning

confidence: 99%

Size control models of Saccharomyces cerevisiae cell proliferation.

Wheals¹

1982

Mol. Cell. Biol.

View full text Add to dashboard Cite

show abstract

“…2A). The result of simulating this model in a proliferating population of cells undergoing 'adder' dynamics [50,51], whereby cells add a constant amount of volume each cell cycle, is presented in Fig. 2.…”

Section: Cell Physiological Models Coupled To Cell Deathmentioning

confidence: 99%

“…We used a stochastic hybrid systems approach [52] to simulate a population of exponentially growing cells undergoing 'adder' dynamics [50,51], whereby cells add a constant amount of volume (K v ) to their initial volume (v 0 ) each cell cycle, which has found recent support in bacteria [53]. Cells are modelled to then divide by stochastically partitioning their volume, with the first daughter inheriting volume and Bj€ orklund as a non-heritable parabolic relationship between mitochondrial functionality (which we interpret as rDC) and cell volume v…”

Section: Mathematical Model Of Power Demand Scaling and Cell Deathmentioning

confidence: 99%

Mitochondrial heterogeneity, metabolic scaling and cell death

et al. 2017

View full text Add to dashboard Cite

Heterogeneity in mitochondrial content has been previously suggested as a major contributor to cellular noise, with multiple studies indicating its direct involvement in biomedically important cellular phenomena. A recently published dataset explored the connection between mitochondrial functionality and cell physiology, where a non-linearity between mitochondrial functionality and cell size was found. Using mathematical models, we suggest that a combination of metabolic scaling and a simple model of cell death may account for these observations. However, our findings also suggest the existence of alternative competing hypotheses, such as a non-linearity between cell death and cell size. While we find that the proposed non-linear coupling between mitochondrial functionality and cell size provides a compelling alternative to previous attempts to link mitochondrial heterogeneity and cell physiology, we emphasise the need to account for alternative causal variables, including cell cycle, size, mitochondrial density and death, in future studies of mitochondrial physiology.

show abstract

“…However, time-lapse studies of single-celled organisms spanning a range of bacteria (4-7) and the yeast Saccharomyces cerevisiae (8) have recently indicated that cell size is regulated by the addition of a fixed volume increment between divisions. Identification of the size regulation behavior constrains the set of feasible molecular scenarios for how growth and division are coordinated with the cell cycle (8)(9)(10). In multicellular tissues, the loss of growth and division/cell cycle coordination could have an impact on the organism's development, yet, to the best of our knowledge, cell growth and size kinetics have never before been measured over generations in a tissue context.…”

mentioning

confidence: 99%

Cell size and growth regulation in the Arabidopsis thaliana apical stem cell niche

Willis

Refahi

Wightman

et al. 2016

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

180

217

View full text Add to dashboard Cite

Cell size and growth kinetics are fundamental cellular properties with important physiological implications. Classical studies on yeast, and recently on bacteria, have identified rules for cell size regulation in single cells, but in the more complex environment of multicellular tissues, data have been lacking. In this study, to characterize cell size and growth regulation in a multicellular context, we developed a 4D imaging pipeline and applied it to track and quantify epidermal cells over 3-4 d in Arabidopsis thaliana shoot apical meristems. We found that a cell size checkpoint is not the trigger for G2/M or cytokinesis, refuting the unexamined assumption that meristematic cells trigger cell cycle phases upon reaching a critical size. Our data also rule out models in which cells undergo G2/M at a fixed time after birth, or by adding a critical size increment between G2/M transitions. Rather, cell size regulation was intermediate between the critical size and critical increment paradigms, meaning that cell size fluctuations decay by ∼75% in one generation compared with 100% (critical size) and 50% (critical increment). Notably, this behavior was independent of local cell-cell contact topologies and of position within the tissue. Cells grew exponentially throughout the first >80% of the cell cycle, but following an asymmetrical division, the small daughter grew at a faster exponential rate than the large daughter, an observation that potentially challenges present models of growth regulation. These growth and division behaviors place strong constraints on quantitative mechanistic descriptions of the cell cycle and growth control.cell size | cell growth | cell cycle | homeostasis | plant stem cells H ow cells coordinate growth and division to achieve a particular cell size remains a fundamental question in biology. Our understanding of this basic property of cells is limited, in part, by the lack of quantitative data on cellular growth and size kinetics over multiple generations, especially in higher eukaryotes (1). Classical studies of cell size homeostasis focused on whether division occurred upon reaching a critical size or after a fixed time period has elapsed (2, 3). However, time-lapse studies of single-celled organisms spanning a range of bacteria (4-7) and the yeast Saccharomyces cerevisiae (8) have recently indicated that cell size is regulated by the addition of a fixed volume increment between divisions. Identification of the size regulation behavior constrains the set of feasible molecular scenarios for how growth and division are coordinated with the cell cycle (8-10). In multicellular tissues, the loss of growth and division/cell cycle coordination could have an impact on the organism's development, yet, to the best of our knowledge, cell growth and size kinetics have never before been measured over generations in a tissue context. The experimental challenges are particularly acute because interdivision times are often on the order of tens of hours, cells have a diversity of shapes necessitating di...

show abstract

Autorepressor Model for Control of DNA Replication

Cited by 174 publications

References 7 publications

Size control models of Saccharomyces cerevisiae cell proliferation.

Size control models of Saccharomyces cerevisiae cell proliferation.

Mitochondrial heterogeneity, metabolic scaling and cell death

Cell size and growth regulation in the Arabidopsis thaliana apical stem cell niche

Contact Info

Product

Resources

About