scholarly journals Geometrical constraints in the scaling relationships between genome size, cell size and cell cycle length in herbaceous plants

2011 ◽  
Vol 279 (1730) ◽  
pp. 867-875 ◽  
Author(s):  
Irena Šímová ◽  
Tomáš Herben

Plant nuclear genome size (GS) varies over three orders of magnitude and is correlated with cell size and growth rate. We explore whether these relationships can be owing to geometrical scaling constraints. These would produce an isometric GS–cell volume relationship, with the GS–cell diameter relationship with the exponent of 1/3. In the GS–cell division relationship, duration of processes limited by membrane transport would scale at the 1/3 exponent, whereas those limited by metabolism would show no relationship. We tested these predictions by estimating scaling exponents from 11 published datasets on differentiated and meristematic cells in diploid herbaceous plants. We found scaling of GS–cell size to almost perfectly match the prediction. The scaling exponent of the relationship between GS and cell cycle duration did not match the prediction. However, this relationship consists of two components: (i) S phase duration, which depends on GS, and has the predicted 1/3 exponent, and (ii) a GS-independent threshold reflecting the duration of the G1 and G2 phases. The matches we found for the relationships between GS and both cell size and S phase duration are signatures of geometrical scaling. We propose that a similar approach can be used to examine GS effects at tissue and whole plant levels.

Molecules ◽  
2021 ◽  
Vol 27 (1) ◽  
pp. 97
Author(s):  
Aneliya Ivanova ◽  
Aleksandar Atemin ◽  
Sonya Uzunova ◽  
Georgi Danovski ◽  
Radoslav Aleksandrov ◽  
...  

Cells have evolved elaborate mechanisms to regulate DNA replication machinery and cell cycles in response to DNA damage and replication stress in order to prevent genomic instability and cancer. The E3 ubiquitin ligase SCFDia2 in S. cerevisiae is involved in the DNA replication and DNA damage stress response, but its effect on cell growth is still unclear. Here, we demonstrate that the absence of Dia2 prolongs the cell cycle by extending both S- and G2/M-phases while, at the same time, activating the S-phase checkpoint. In these conditions, Ctf4—an essential DNA replication protein and substrate of Dia2—prolongs its binding to the chromatin during the extended S- and G2/M-phases. Notably, the prolonged cell cycle when Dia2 is absent is accompanied by a marked increase in cell size. We found that while both DNA replication inhibition and an absence of Dia2 exerts effects on cell cycle duration and cell size, Dia2 deficiency leads to a much more profound increase in cell size and a substantially lesser effect on cell cycle duration compared to DNA replication inhibition. Our results suggest that the increased cell size in dia2∆ involves a complex mechanism in which the prolonged cell cycle is one of the driving forces.


Genome ◽  
1999 ◽  
Vol 42 (2) ◽  
pp. 361-362 ◽  
Author(s):  
Alexander E Vinogradov

At a certain temperature, which is a compromise for temperatures at which the species are adapted, the relationship between genome size and cell cycle duration during synchronous cleavage divisions can be very strong (r = 1.00, P < 0.01) in four closely related frogs, suggesting a functional dependence.Key words: genome size, genome evolution, genome cytoecology, noncoding DNA, cell cycle duration.


1980 ◽  
Vol 85 (1) ◽  
pp. 108-115 ◽  
Author(s):  
C J Rivin ◽  
W L Fangman

When the growth rate of the yeast Saccharomyces cerevisiae is limited with various nitrogen sources, the duration of the S phase is proportional to cell cycle length over a fourfold range of growth rates (C.J. Rivin and W. L. Fangman, 1980, J. Cell Biol. 85:96-107). Molecular parameters of the S phases of these cells were examined by DNA fiber autoradiography. Changes in replication fork rate account completely for the changes in S-phase duration. No changes in origin-to-origin distances were detected. In addition, it was found that while most adjacent replication origins are activated within a few minutes of each other, new activations occur throughout the S phase.


2009 ◽  
Vol 29 (15) ◽  
pp. 4025-4032 ◽  
Author(s):  
Lee Kiang ◽  
Christian Heichinger ◽  
Stephen Watt ◽  
Jürg Bähler ◽  
Paul Nurse

ABSTRACT To achieve faithful replication of the genome once in each cell cycle, reinitiation of S phase is prevented in G2 and origins are restricted from refiring within S phase. We have investigated the block to rereplication during G2 in fission yeast. The DNA synthesis that occurs when G2/M cyclin-dependent kinase (CDK) activity is depleted has been assumed to be repeated rounds of S phase without mitosis, but this has not been demonstrated to be the case. We show here that on G2/M CDK depletion in G2, repeated S phases are induced, which are correlated with normal G1/S transcription and attainment of doublings in cell size. Mostly normal mitotic S-phase origins are utilized, although at different efficiencies, and replication is essentially equal across the genome. We conclude that CDK inhibits reinitiation of S phase during G2, and if G2/M CDK is depleted, replication results from induction of a largely normal S-phase program with only small differences in origin usage and efficiency.


2006 ◽  
Vol 26 (12) ◽  
pp. 4701-4711 ◽  
Author(s):  
Courtney G. Havens ◽  
Alan Ho ◽  
Naohisa Yoshioka ◽  
Steven F. Dowdy

ABSTRACT Proliferating cells have a higher metabolic rate than quiescent cells. To investigate the role of metabolism in cell cycle progression, we examined cell size, mitochondrial mass, and reactive oxygen species (ROS) levels in highly synchronized cell populations progressing from early G1 to S phase. We found that ROS steadily increased, compared to cell size and mitochondrial mass, through the cell cycle. Since ROS has been shown to influence cell proliferation and transformation, we hypothesized that ROS could contribute to cell cycle progression. Antioxidant treatment of cells induced a late-G1-phase cell cycle arrest characterized by continued cellular growth, active cyclin D-Cdk4/6 and active cyclin E-Cdk2 kinases, and inactive hyperphosphorylated pRb. However, antioxidant-treated cells failed to accumulate cyclin A protein, a requisite step for initiation of DNA synthesis. Further examination revealed that cyclin A continued to be ubiquitinated by the anaphase promoting complex (APC) and to be degraded by the proteasome. This antioxidant arrest could be rescued by overexpression of Emi1, an APC inhibitor. These observations reveal an intrinsic late-G1-phase checkpoint, after transition across the growth factor-dependent G1 restriction point, that links increased steady-state levels of endogenous ROS and cell cycle progression through continued activity of APC in association with Cdh1.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Nicolas Talarek ◽  
Elisabeth Gueydon ◽  
Etienne Schwob

How cells coordinate growth and division is key for size homeostasis. Phosphorylation by G1-CDK of Whi5/Rb inhibitors of SBF/E2F transcription factors triggers irreversible S-phase entry in yeast and metazoans, but why this occurs at a given cell size is not fully understood. We show that the yeast Rim15-Igo1,2 pathway, orthologous to Gwl-Arpp19/ENSA, is up-regulated in early G1 and helps promoting START by preventing PP2ACdc55 to dephosphorylate Whi5. RIM15 overexpression lowers cell size while IGO1,2 deletion delays START in cells with low CDK activity. Deletion of WHI5, CDC55 and ectopic CLN2 expression suppress the START delay of igo1,2∆ cells. Rim15 activity increases after cells switch from fermentation to respiration, where Igo1,2 contribute to chromosome maintenance. Interestingly Cln3-Cdk1 also inhibits Rim15 activity, which enables homeostatic control of Whi5 phosphorylation and cell cycle entry. We propose that Rim15/Gwl regulation of PP2A plays a hitherto unappreciated role in cell size homeostasis during metabolic rewiring of the cell cycle.


1982 ◽  
Vol 57 (1) ◽  
pp. 315-329
Author(s):  
C.D. Rasmussen ◽  
J.D. Berger

Two temperature-sensitive cell-cycle mutants were used to generate abnormally large cells (size estimated by protein content) with either normal or increased DNA contents. The first mutant, cc1, blocks DNA synthesis, but allows cell growth at the restrictive temperature. The cells do not progress through the cell cycle while at the restrictive temperature, but do recover and complete the cell cycle when returned to permissive conditions. The progeny have increased cell size and normal DNA content. Downward regulation of cell size occurs during the ensuing cell cycle at permissive temperature. Two processes are involved. First, the G1 period is reduced or eliminated. As initial cell size increases there is a progressive shortening of the cell cycle to 75% of normal. This limit cell-cycle duration is reached when the initial mass of the cell is equal to or greater than that of normal cells at the time of DNA synthesis initiation (0.25 of a cell cycle). Cells with the limit cell cycle begin macronuclear DNA synthesis immediately after fission. The durations of the S period and fission are normal. Second, the rate of cell growth is unaffected by the increase in cell size, and results in the partitioning of excess cell mass between the daughter cells at the next fission. The second mutant, cc2, blocks cell division, but allows DNA synthesis to occur at a reduced rate so that cells with up to about 140% of the normal initial DNA content and twice the normal cell mass can be produced. The pattern of cell-cycle shortening is the same as in ccl. The rates of growth and both the rate and amount of DNA synthesis are proportional to the initial DNA content. This suggests that the rates of growth and DNA synthesis are limited by the transcriptional activity of the macronucleus in both cc1 and cc2 cells when they begin the cell cycle with experimentally increased cell mass. Increases in both cell size and initial DNA content are required to bring about increases in the rates of growth and DNA accumulation.


1984 ◽  
Vol 68 (1) ◽  
pp. 95-111
Author(s):  
A. Gangopadhyay ◽  
S. Chatterjee

The treatment of Amoeba indica with ethylmethanesulphonate (EMS) at early S, late S and late G2 phases of the cell cycle leads to the production of mini amoeba cells in the G2 period. Among them, only a few of the mini cells that originated from EMS treatment at early S phase have been found to be viable and to give rise to stable clones. These mini amoebae show stable and altered characteristic features in cell size, structure, membrane properties, cell-cycle timing and the patterns of macromolecular syntheses as compared to the parental cells. It is suggested that the mini amoeba cell is a size mutant that has a cell-cycle-phase-specific origin. The finding is discussed in relation to preferential mutagenic action involving the functional state of DNA leading to the production of viable mutant amoebae.


2021 ◽  
Author(s):  
Taras Pasternak ◽  
Stefan Kircher ◽  
Klaus Palme

AbstractRoot development is a complex spatial-temporal process that originates in the root apical meristem (RAM). To keep the organ’s shape in harmony, the different cell files’ growth must be coordinated. Thereby, diverging kinetics of cell growth in these files may be obtained not only by differential cell growth but also by local differences in cell proliferation frequency. Understanding potential local differences in cell cycle duration in the RAM requires a quantitative estimation of the underlying mitotic cell cycle phases’ timing at every cell file and every position. However, so far, precise methods for such analysis are missing.This study presents a robust and straightforward method to determine the duration of the cell cycle’s key stages in all cell layers in a plant’s root simultaneously. The technique combines marker-free experimental techniques based on detection of incorporation of 5-ethynyl-2’-deoxyuridine (EdU) and mitosis with a high-resolution plant phenotyping platform to analyze all key cell cycle events’ kinetics.In the Arabidopsis thaliana L. RAM S-phase duration was found to be as short as 18-20 minutes in all cell files. But subsequent G2-phase duration depends on the cell type/position and varies from 3,5 hours in the pericycle to more than 4,5 hours in the epidermis. Overall, S+G2+M duration in Arabidopsis under our condition is 4 hours in the pericycle and up to 5,5 hours in the epidermis.Endocycle duration was determined as the time required to achieve 100% EdU index in the transition zone and estimated as 3-4 hours.Besides Arabidopsis, we show that the presented technique is applicable also to root tips of other dicot and monocot plants (tobacco (Nicotiana tabacum L.), tomato (Lycopersicon esculentum L.) and wheat (Triticum aestivum L.)).


2015 ◽  
Vol 524 (3) ◽  
pp. 456-470 ◽  
Author(s):  
Miguel Turrero García ◽  
YoonJeung Chang ◽  
Yoko Arai ◽  
Wieland B. Huttner

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