A Amon

A Bardin

A Ciliberto

A Goldbeter

A Skirycz

Alistair J. P. Brown

C Dahmann

C Epstein

Celso Grebogi

CL Theesfeld

D Lew

D McCollum

D Morgan

Despoina Kaloriti

DJ Lew

E Nigg

E Schwob

E Traverso

Elahe Radmaneshfar

F Cross

F Stegmeier

G Bellí

G Yaakov

H Claeys

H Saito

J Brewster

J Clotet

J McMillan

JL Burton

K Chen

KJ Simpson-Lavy

L Dirick

M Adrover

M Alexander

M Barberis

M Gustin

M Mendenhall

M Tyers

M. Carmen Romano

Marco Thiel

Michael C. Gustin

Michael Polymenis

N Grandin

Neil A. R. Gow

P Nash

P Nurse

R Sia

R Venta

R Verma

RN Booher

S Chandrasekaran

S Ghaemmaghami

S Jaspersen

S Jensen

S Piatti

T Su

U Surana

V Nguyen

V Reiser

W Zachariae

X Escoté

Z Zi

PLoS ONE

English

PubMed

The cell cycle is a sequence of biochemical events that are controlled by complex but robust molecular machinery. This enables cells to achieve accurate self-reproduction under a broad range of different conditions. Environmental changes are transmitted by molecular signalling networks, which coordinate their action with the cell cycle. The cell cycle process and its responses to environmental stresses arise from intertwined nonlinear interactions among large numbers of simpler components. Yet, understanding of how these pieces fit together into a coherent whole requires a systems biology approach. Here, we present a novel mathematical model that describes the influence of osmotic stress on the entire cell cycle ofﾠS. cerevisiaefor the first time. Our model incorporates all recently known and several proposed interactions between the osmotic stress response pathway and the cell cycle. This model unveils the mechanisms that emerge as a consequence of the interaction between the cell cycle and stress response networks. Furthermore, it characterises the role of individual components. Moreover, it predicts different phenotypical responses for cells depending on the phase of cells at the onset of the stress. The key predictions of the model are: (i) exposure of cells to osmotic stress during the late S and the early G2/M phase can induce DNA re-replication before cell division occurs, (ii) cells stressed at the late G2/M phase display accelerated exit from mitosis and arrest in the next cell cycle, (iii) osmotic stress delays the G1-to-S and G2-to-M transitions in a dose dependent manner, whereas it accelerates the M-to-G1 transition independently of the stress dose and (iv) the Hog MAPK network compensates the role of the MEN network during cell division of MEN mutant cells. These model predictions are supported by independent experiments inﾠS. cerevisiaeﾠand, moreover, have recently been observed in other eukaryotes

Radmaneshfar, Elahe

Kaloriti, Despoina

Gustin, Michael C.

Gow, Neil A.R.

Brown, Alistair J.P.

Grebogi, Celso

Romano, M.Carmen

Thiel, Marco

Rice University Research Repository

From START to FINISH: The Influence of Osmotic Stress on the Cell Cycle

Gow, Neil A. R.

Brown, Alistair J. P.

Romano, Maria Carmen

FreiDok plus

Gustin, Michael C

Gow, Neil A R

Brown, Alistair J P

Romano, M Carmen

Aberdeen University Research

A late mitotic regulatory network controlling cyclin destruction in Saccharomyces cerevisiae.

A low number of SIC1 mrna molecules ensures a low noise level in cell cycle progression of budding yeast.

A monitor for bud emergence in the yeast morphogenesis checkpoint.

A quantitative study of the Hog1 MAPK response to uctuating osmotic stress in Saccharomyces cerevisiae.

Activation of S-phasepromoting CDKs in late G1 defines a ‘point of no return’ after which Cdc6 synthesis cannot promote DNA replication in yeast.

Amon A

An amplified sensitivity arising from covalent modification in biological systems.

An osmosensing signal transduction pathway in yeast.

be an upstream activator of Cln1, Cln2 and other cyclins.

Cdc28 tyrosine phosphorylation and the morphogenesis checkpoint in budding yeast.

Cell size at S phase initiation: An emergent property of the G1/S network. PLoS

Cell-cycle checkpoints that ensure coordination between nuclear and cytoplasmic events in Saccharomyces cerevisiae.

Characterisation of the Net1 cell cycle-dependent regulator of the Cdc14 phosphatase from budding yeast.

CLB5 and CLB6, a new pair of b cyclins involved

Control of Swe1p degradation by the morphogenesis checkpoint.

Cyclin-dependent kinases prevent DNA rereplication through multiple mechanisms.

Cyclin-dependent protein kinases: Key regulators of the eukaryotic cell cycle.

DELLA signalling mediates stress-induced cell differentiation in Arabidopsis leaves through modulation of APC/C activity.

Double-negative feedback between S-phase cyclin-CDK and CKI generates abruptness in the G1/S switch. Frontiers

Genes that can bypass the CLN requirement for Saccharomyces cerevisiae cell cycle START.

Global analysis of protein expression in yeast.

Hodge A

Hog1 mediates cell-cycle arrest in G1 phase by the dual targeting of Sic1.

Hsl1p, a Swe1p inhibitor, is degraded via the anaphase-promoting complex.

Integrative analysis of cell cycle control in budding yeast.

Kinetic analysis of a molecular model of the budding yeast cell cycle.

MAP kinase pathways in the yeast Saccharomyces cerevisiae.

Mathematical model of the morphogenesis checkpoint in budding yeast.

Mechanisms that help the yeast cell cycle clock tick: G2 cyclins transcriptionally activate G2 cyclins and repress G1 cyclins.

Mitotic exit: delaying the end without FEAR.

Morphogenesis in the yeast cell cycle: regulation by Cdc28 and cyclins.

Multisite phosphorylation of a CDK inhibitor sets a threshold for the onset of DNA replication.

Osmotic stress causes a G1 cell cycle delay and downregulation of Cln3/Cdc28 activity in Saccharomyces cerevisiae.

Pause-andstop: The effects of osmotic stress on cell proliferation during early leaf development in Arabidopsis and a role for ethylene signalling in cell cycle arrest.

Phosphorylation of Sic1p by G1 Cdk required for its degradation and entry into S phase.

Properties of Saccharomyces cerevisiae wee1 and its differential regulation of p34CDC28 in response to G1 and G2 cyclins.

Qualifying for the license to replicate.

Quantitative characterization of a mitotic cyclin threshold regulating exit from mitosis.

Regulation of cell cycle progression by Swe1p and Hog1p following hypertonic stress.

Regulation of the APC and the exit from mitosis.

Regulation of the eukaryotic cell cycle.

required for proper stress responses of S.

Response to hyperosmotic stress.

Roles and regulation of Cln-Cdc28 kinases at the start of the cell cycle of Saccharomyces cerevisiae.

S-phase-promoting cyclin-dependent kinases prevent re-replication by inhibiting the transition of replication origins to a pre-replicative state.

Sic1 plays a role in timing and oscillatory behaviour of B-type cyclins.

Stress-stimulated mitogenactivated protein kinases control the stability and activity of the Cdt1 DNA replication licensing factor.

Testing a mathematical model of the yeast cell cycle.

The morphogenesis checkpoint in Saccharomyces cerevisiae: cell cycle control of

The morphogenesis checkpoint: how yeast cells watch their figures.

The role of CDC28 and cyclins during mitosis in the budding yeast S.

The stressactivated protein kinase Hog1 mediates S phase delay in response to osmostress.

Timedependent quantitative multicomponent control of the G1-S network by the stress-activated protein kinase Hog1 upon osmostress.

Timing is everything: regulation of mitotic exit and cytokinesis by the MEN and SIN.

Whose end is destruction: Cell division and the anaphasepromoting complex.

From START to FINISH : the influence of osmotic stress on the cell cycle

The cell cycle is a sequence of biochemical events that are controlled by complex but robust molecular machinery. This enables cells to achieve accurate self-reproduction under a broad range of different conditions. Environmental changes are transmitted by molecular signalling networks, which coordinate their action with the cell cycle. The cell cycle process and its responses to environmental stresses arise from intertwined nonlinear interactions among large numbers of simpler components. Yet, understanding of how these pieces fit together into a coherent whole requires a systems biology approach. Here, we present a novel mathematical model that describes the influence of osmotic stress on the entire cell cycle of S. cerevisiae for the first time. Our model incorporates all recently known and several proposed interactions between the osmotic stress response pathway and the cell cycle. This model unveils the mechanisms that emerge as a consequence of the interaction between the cell cycle and stress response networks. Furthermore, it characterises the role of individual components. Moreover, it predicts different phenotypical responses for cells depending on the phase of cells at the onset of the stress. The key predictions of the model are: (i) exposure of cells to osmotic stress during the late S and the early G2/M phase can induce DNA re-replication before cell division occurs, (ii) cells stressed at the late G2/M phase display accelerated exit from mitosis and arrest in the next cell cycle, (iii) osmotic stress delays the G1-to-S and G2-to-M transitions in a dose dependent manner, whereas it accelerates the M-to-G1 transition independently of the stress dose and (iv) the Hog MAPK network compensates the role of the MEN network during cell division of MEN mutant cells. These model predictions are supported by independent experiments in S. cerevisiae and, moreover, have recently been observed in other eukaryotes

Michael C Gustin

Neil A R Gow

Alistair J P Brown

M Carmen Romano

Directory of Open Access Journals

From START to FINISH: the influence of osmotic stress on the cell cycle.

Radmaneshfar Elahe

Kaloriti Despoina

Gustin Michael C.

Gow Neil A. R.

Brown Alistair J. P.

Grebogi Celso

Romano M. Carmen

Thiel Marco

Public Library of Science (PLOS)

<div><p>The cell cycle is a sequence of biochemical events that are controlled by complex but robust molecular machinery. This enables cells to achieve accurate self-reproduction under a broad range of different conditions. Environmental changes are transmitted by molecular signalling networks, which coordinate their action with the cell cycle. The cell cycle process and its responses to environmental stresses arise from intertwined nonlinear interactions among large numbers of simpler components. Yet, understanding of how these pieces fit together into a coherent whole requires a systems biology approach. Here, we present a novel mathematical model that describes the influence of osmotic stress on the entire cell cycle of <i>S. cerevisiae</i> for the first time. Our model incorporates all recently known and several proposed interactions between the osmotic stress response pathway and the cell cycle. This model unveils the mechanisms that emerge as a consequence of the interaction between the cell cycle and stress response networks. Furthermore, it characterises the role of individual components. Moreover, it predicts different phenotypical responses for cells depending on the phase of cells at the onset of the stress. The key predictions of the model are: (i) exposure of cells to osmotic stress during the late S and the early G2/M phase can induce DNA re-replication before cell division occurs, (ii) cells stressed at the late G2/M phase display accelerated exit from mitosis and arrest in the next cell cycle, (iii) osmotic stress delays the G1-to-S and G2-to-M transitions in a dose dependent manner, whereas it accelerates the M-to-G1 transition independently of the stress dose and (iv) the Hog MAPK network compensates the role of the MEN network during cell division of MEN mutant cells. These model predictions are supported by independent experiments in <i>S. cerevisiae</i> and, moreover, have recently been observed in other eukaryotes.</p></div

From START to FINISH : the influence of osmotic stress on the cell cycle

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Aberdeen University Research

Directory of Open Access Journals

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