Goldbeter2013-Oscillatory activity of cyclin-dependent kinases in the cell cycle
Ontology highlight
ABSTRACT:
SUBMITTER: 
Ahmad Zyoud
PROVIDER: BIOMD0000000944 | BioModels | 2024-09-02
REPOSITORIES: BioModels
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Oscillatory enzyme reactions and Michaelis-Menten kinetics.
FEBS letters 20130723 17
Oscillations occur in a number of enzymatic systems as a result of feedback regulation. How Michaelis-Menten kinetics influences oscillatory behavior in enzyme systems is investigated in models for oscillations in the activity of phosphofructokinase (PFK) in glycolysis and of cyclin-dependent kinases in the cell cycle. The model for the PFK reaction is based on a product-activated allosteric enzyme reaction coupled to enzymatic degradation of the reaction product. The Michaelian nature of the pr ...[more]
Similar Datasets
Project description:Goldbeter1991 - Min Mit Oscil
Minimal cascade model for the mitotic oscillator involving cyclin and cdc2 kinase.
This model has been generated by MathSBML 2.4.6 (14-January-2005) 14-January-2005 18:33:39.806932.
This model is described in the article:
A minimal cascade model for the mitotic oscillator involving cyclin and cdc2 kinase.
Goldbeter A.
Proc. Natl. Acad. Sci. U.S.A. 1991; 88(20):9107-11
Abstract:
A minimal model for the mitotic oscillator is presented. The model, built on recent experimental advances, is based on the cascade of post-translational modification that modulates the activity of cdc2 kinase during the cell cycle. The model pertains to the situation encountered in early amphibian embryos, where the accumulation of cyclin suffices to trigger the onset of mitosis. In the first cycle of the bicyclic cascade model, cyclin promotes the activation of cdc2 kinase through reversible dephosphorylation, and in the second cycle, cdc2 kinase activates a cyclin protease by reversible phosphorylation. That cyclin activates cdc2 kinase while the kinase triggers the degradation of cyclin has suggested that oscillations may originate from such a negative feedback loop [Félix, M. A., Labbé, J. C., Dorée, M., Hunt, T. & Karsenti, E. (1990) Nature (London) 346, 379-382]. This conjecture is corroborated by the model, which indicates that sustained oscillations of the limit cycle type can arise in the cascade, provided that a threshold exists in the activation of cdc2 kinase by cyclin and in the activation of cyclin proteolysis by cdc2 kinase. The analysis shows how miototic oscillations may readily arise from time lags associated with these thresholds and from the delayed negative feedback provided by cdc2-induced cyclin degradation. A mechanism for the origin of the thresholds is proposed in terms of the phenomenon of zero-order ultrasensitivity previously described for biochemical systems regulated by covalent modification.
This model is hosted on BioModels Database
and identified by: BIOMD0000000003
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
2024-09-02 | BIOMD0000000003 | BioModels
Project description:Goldbeter1991 - Min Mit Oscil, Expl Inact
This model represents the inactive forms of CDC-2 Kinase and Cyclin Protease as separate species, unlike the ODEs in the published paper, in which the equations for the inactive forms are substituted into the equations for the active forms using a mass conservation rule M+MI=1,X+XI=1. Mass is still conserved in this model through the explicit reactions MMI and XXI. The terms in the kinetic laws are identical to the corresponding terms in the kinetic laws in the published paper.
This model has been generated by MathSBML 2.4.6 (14-January-2005) 14-January-2005 18:37:35.503857.
This model is described in the article:
A minimal cascade model for the mitotic oscillator involving cyclin and cdc2 kinase.
Goldbeter A.
Proc. Natl. Acad. Sci. USA 1991 Oct; 88(20):9107-11
Abstract:
A minimal model for the mitotic oscillator is presented. The model, built on recent experimental advances, is based on the cascade of post-translational modification that modulates the activity of cdc2 kinase during the cell cycle. The model pertains to the situation encountered in early amphibian embryos, where the accumulation of cyclin suffices to trigger the onset of mitosis. In the first cycle ofthe bicyclic cascade model, cyclin promotes the activation of cdc2 kinase through reversible dephosphorylation, and in the second cycle, cdc2 kinase activates a cyclin protease by reversible phosphorylation. That cyclin activates cdc2 kinase while the kinase triggers the degradation of cyclin has suggested that oscillations may originate from such a negative feedback loop [Félix, M. A., Labbé, J. C., Dorée, M., Hunt, T. & Karsenti, E. (1990) Nature (London) 346, 379-382]. Thisconjecture is corroborated by the model, which indicates that sustained oscillations of the limit cycle type can arise in the cascade, provided that a threshold exists in the activation of cdc2 kinase by cyclin and in the activation of cyclinproteolysis by cdc2 kinase. The analysis shows how miototic oscillations may readily arise from time lags associated with these thresholds and from the delayed negative feedback provided by cdc2-induced cyclin degradation. A mechanism for theorigin of the thresholds is proposed in terms of the phenomenon of zero-order ultrasensitivity previously described for biochemical systems regulated by covalent modification.
This model is hosted on BioModels Database
and identified by: BIOMD0000000004
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
2024-09-02 | BIOMD0000000004 | BioModels
Project description:We consider a minimal cascade model previously proposed for the mitotic oscillator driving the embryonic cell division cycle. The model is based on a bicyclic phosphorylation-dephosphorylation cascade involving cyclin and cdc2 kinase. By constructing stability diagrams showing domains of periodic behavior as a function of the maximum rates of the kinases and phosphatases involved in the two cycles of the cascade, we investigate the role of these converter enzymes in the oscillatory mechanism. Oscillations occur when the balance of kinase and phosphatase rates in each cycle is in a range bounded by two critical values. The results suggest ways to arrest the mitotic oscillator by altering the maximum rates of the converter enzymes. These results bear on the control of cell proliferation.
2024-09-02 | BIOMD0000000729 | BioModels
Project description:Oscillatory phenomena are ubiquitous across different biological scales, from individual cells to tissues and whole organisms. In physical systems, oscillatory behaviour can emerge from weak coupling of independent stochastic elements. Once established, oscillations can drive coordinated group behaviour and encode robust information through oscillation frequency or amplitude. Here we use experimentation and modelling to understand the emergence and information coding properties of oscillatory cyclic adenosine monophosphate (cAMP) signaling in D. discoideum. Oscillatory cAMP signaling drives aggregation of individual amoebae and coordinated temporal shifts in gene expression. However, it is unknown how the collective behaviour emerges and attenuates in an auto-regulatory manner where temporal transcriptional regulation must decode variation in cAMP pulse count, frequency, or amplitude. To address these questions, we identified a transcription factor, Hbx5, that is essential for the initiation of collective behaviour and its activity provides a single-cell readout of the earliest sign of cAMP signaling. This reveals stochastic pulses in cAMP signaling precede collective oscillations, with Hbx5 dependent transcriptional feedback enhancing signal sensitivity necessary for the emergence of collective oscillations. We demonstrate that once collective oscillations have been established, another cAMP-regulated transcription factor, GtaC, required for subsequent developmental progression becomes activated. Modelling and experimentation suggest that temporal differences in transcription factor activation arise from differences in the threshold at which the protein kinase, ErkB, influences their activity. This leads us to propose that changes in the amplitude of cAMP oscillations during development encode temporal information, driving the orderly progression of development. These studies thus provide crucial insights into the principles driving collective behaviour and the evolution of multicellular systems.
2024-10-29 | GSE272520 | GEO
Project description:We report that inactivation of the fission yeast Cdk7 kinase affects gene expression through both its RNA Polymerase II CTD kinase activity and its Cdc2-activating kinase activity. The ribosome biogenesis cluster is specifically downregulated when Cdc2 T167 phosphorylation is abolished, which results is slow growth. We propose that Cdc2 activation by CAK defines the rate change point observed in mid G2 and that CAK therefore couples cell growth to cell division. Total RNA was isolated from two biological replicates for all conditions, and each biological replicate was hybridized in duplicate on Agilent arrays (dye-swap).
2012-02-19 | E-GEOD-27425 | biostudies-arrayexpress
Project description:We report the presence of extensive, transcriptionally controlled oscillations in the C. elegans, developmental transcriptome. Furthermore, using ribosome profiling, we show that these oscillating transcripts are actively translated.
2014-03-01 | GSE52905 | GEO
Project description:Brain oscillations are remarkable components of brain activity that support memory encoding. However, it remains a major challenge to determine the molecular mechanisms underlining this activity in humans. Here, we used direct intracranial electroencephalography recordings from patients performing free recall tasks of verbal memory encoding in temporal cortex. Using resected tissue transcriptomics from the same patients, we linked gene expression with brain oscillations, identifying genes correlated with oscillatory signatures of memory formation across six frequency bands. Co-expression analysis isolated biomarker-specific modules associated with neuropsychiatric disorders as well as ion channel activity. Using single-nuclei transcriptomic data from resected tissue, we further revealed that biomarker-specific modules are enriched for both excitatory and inhibitory neurons. This unprecedented dataset of patient-specific brain oscillations coupled to genomics unlocks new insights into the genetic mechanisms that support memory encoding. By linking brain expression of these genes to oscillatory patterns, our data help overcome limitations of phenotypic methods to uncover genetic links to memory performance.
2020-12-09 | GSE139914 | GEO
Project description:Kholodenko2000 - Ultrasensitivity and negative feedback bring oscillations in MAPK cascade
The combination of ultrasensitivity and negative feedback bring sustained oscillations in the mitogen-activated protein kinase cascades.
This model is described in the article:
Negative feedback and ultrasensitivity can bring about oscillations in the mitogen-activated protein kinase cascades.
Kholodenko BN
Eur. J. Biochem. 2000; 267(6):1583-8
Abstract:
Functional organization of signal transduction into protein phosphorylation cascades, such as the mitogen-activated protein kinase (MAPK) cascades, greatly enhances the sensitivity of cellular targets to external stimuli. The sensitivity increases multiplicatively with the number of cascade levels, so that a tiny change in a stimulus results in a large change in the response, the phenomenon referred to as ultrasensitivity. In a variety of cell types, the MAPK cascades are imbedded in long feedback loops, positive or negative, depending on whether the terminal kinase stimulates or inhibits the activation of the initial level. Here we demonstrate that a negative feedback loop combined with intrinsic ultrasensitivity of the MAPK cascade can bring about sustained oscillations in MAPK phosphorylation. Based on recent kinetic data on the MAPK cascades, we predict that the period of oscillations can range from minutes to hours. The phosphorylation level can vary between the base level and almost 100% of the total protein. The oscillations of the phosphorylation cascades and slow protein diffusion in the cytoplasm can lead to intracellular waves of phospho-proteins.
This model is hosted on BioModels Database
and identified by: BIOMD0000000010
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
2024-09-02 | BIOMD0000000010 | BioModels
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2021-06-30 | MTBLS2795 | MetaboLights
Project description:We report the presence of extensive, transcriptionally controlled oscillations in the C. elegans, developmental transcriptome. Furthermore, using ribosome profiling, we show that these oscillating transcripts are actively translated. Ribosome-profiling analysis of a timecourse that was collected over C. elegans development
2014-03-01 | E-GEOD-52905 | biostudies-arrayexpress