Circadian rhythms and protein turnover: The effect of temperature on the period lengths of clock mutants simulated by the Goodwin oscillator

Ruoff, Peter; Mohsenzadeh, Saadat; Rensing, Ludger

doi:10.1007/bf01141953

Cited by 47 publications

(30 citation statements)

References 29 publications

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“…In accordance with these predictions, the half-life of FRQ 7 has been found to be approximately twice as long as the wild-type FRQ þ half-life (19). In addition, Liu et al (20) have recently shown, by blocking certain phosphorylation sites in FRQ, that an increased stability of FRQ leads to an increase of the period length, precisely as predicted by the Goodwin model (18).…”

Section: Introductionsupporting

confidence: 62%

“…Both short and long period alleles at the frq locus are known, the long period mutant frq 7 showing an impaired temperature-compensation (17). The loss of temperature-compensation in frq 7 may be explained by a more stable FRQ 7 protein with an increased activation energy in FRQ 7 -degradation (18). In accordance with these predictions, the half-life of FRQ 7 has been found to be approximately twice as long as the wild-type FRQ þ half-life (19).…”

Section: Introductionmentioning

confidence: 99%

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Circadian period lengths of lipid synthesis mutants (cel,chol-1) ofNeurosporashow defective temperature, but intact pH-compensation

Ruoff

Slewa

2002

Chronobiology International

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The influence of extracellular pH on the circadian sporulation rhythm of Neurospora crassa has been investigated for the mutants chol-1 and cel. Both mutants have a defect in the lipid synthesis pathway and require either choline or palmitate, respectively, as supplements for normal growth. The chol-1 and cel mutants also show an impaired temperature-compensation when growing on minimal medium. We investigated the possible correlation between loss of temperature-and pH-compensation in cel and chol-1 similar to the correlation found earlier for the frq 7 mutant. Our results show that the cel and the chol-1 mutants, although defective in temperature-compensation have an intact pH-compensation of their circadian rhythms. At present, the products of the frq-locus are the only components of the clock that affect the sporulation rhythm of Neurospora both through pH-and temperature-compensation.

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Section: Introductionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Circadian period lengths of lipid synthesis mutants (cel,chol-1) ofNeurosporashow defective temperature, but intact pH-compensation

Ruoff

Slewa

2002

Chronobiology International

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“…5), the major difference between HT and PS models has not been reported or investigated, to our knowledge. Future work can also investigate whether PS models follow the entrainment properties [37,45,47,142,[156][157][158] or temperature compensation mechanisms [38,40,42,[159][160][161][162][163][164][165][166] identified with HT models. Furthermore, stochastic simulations of HT models commonly indicate that circadian clocks can maintain rhythms even with low numbers of molecules [167][168][169][170].…”

Section: Resultsmentioning

confidence: 99%

“…Following the Goodwin model (Eqs. 1 and 2), the Hill function has been widely used to describe transcriptional repression in other molecular circadian clock models (HT models) of diverse organisms: Neurospora [38][39][40], Drosophila [32,[41][42][43][44][45][46] and mammals [47][48][49][50][51][52][53].…”

Section: Introductionmentioning

confidence: 99%

Protein sequestration versus Hill‐type repression in circadian clock models

Kim¹

2016

IET syst. biol.

107

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Circadian (~24hr) clocks are self-sustained endogenous oscillators with which organisms keep track of daily and seasonal time. Circadian clocks frequently rely on interlocked transcriptionaltranslational feedback loops to generate rhythms that are robust against intrinsic and extrinsic perturbations. To investigate the dynamics and mechanisms of the intracellular feedback loops in circadian clocks, a number of mathematical models have been developed. The majority of the models use Hill functions to describe transcriptional repression in a way that is similar to the Goodwin model. Recently, a new class of models with protein sequestration-based repression has been introduced. Here, we discuss how this new class of models differs dramatically from those based on Hill-type repression in several fundamental aspects: conditions for rhythm generation, robust network designs and the periods of coupled oscillators. Consistently, these fundamental properties of circadian clocks also differ among Neurospora, Drosophila, and mammals depending on their key transcriptional repression mechanisms (Hill-type repression or protein sequestration). Based on both theoretical and experimental studies, this review highlights the importance of careful modeling of transcriptional repression mechanisms in molecular circadian clocks.

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“…The Goodwin model [115,116] is even simpler, with only one nonlinearity located at the transcription inhibition stage, but with a higher Hill coefficient (n = 9), and the representation of RNA degradation by a linear term (versus Michaelis-Menten in the LeloupGoldebeter model). Nevertheless, it proves useful when studying the behaviour of the clock under the influence of external inputs, such as temperature compensation [235] or (with an extension to include polyphosphorylations, as in the Leloup-Goldbeter model of P ER oscillations) of genetic mutations [262]. …”

mentioning

confidence: 99%

Modelling Physiological and Pharmacological Control on Cell Proliferation to Optimise Cancer Treatments

Clairambault

2009

Math. Model. Nat. Phenom.

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Abstract. This review aims at presenting a synoptic, if not exhaustive, point of view on some of the problems encountered by biologists and physicians who deal with natural cell proliferation and disruptions of its physiological control in cancer disease. It also aims at suggesting how mathematicians are naturally challenged by these questions and how they might help, not only biologists to deal theoretically with biological complexity, but also physicians to optimise therapeutics, on which last point the focus will be set here. To this purpose, mathematical modelling should represent proliferating cell population dynamics with natural built-in control targets (which implies modelling the cell division cycle), together with the distribution of drugs in the organism and their molecular actions on different targets at the cell level on proliferation, i.e., molecular pharmacokinetics-pharmacodynamics of antiproliferative drugs. This should make possible optimal control of drug delivery with constraints to be determined according to the main pharmacological issues encountered in the clinic: unwanted toxic side-effects, occurrence of drug resistance. Mathematical modelling should also take into account physiological determinants of cell and tissue proliferation, such as intervention of the immune system, circadian control on cell cycle checkpoint proteins, and activity of intracellular drug processing enzymes together with individual variations in the activities of these proteins (genetic polymorphism). Taking these points into account will add to the rich scenery of normal or disrupted cell and tissue regulations, and their corrections by drugs, a natural environmental, whole body physiological, frame. It is necessary indeed to consider such a framework if one wants to eventually be actually helpful to clinicians who routinely treat by combinations of drugs living Humans with their complex whole body regulations, often dependent on genotypic variations, and not isolated cells or tissues.Key words: cell proliferation, population dynamics, physiologically structured partial differential equations, pharmacological control, pharmacokinetics-pharmacodynamics, physiological modelling, cancer treatments, therapeutic optimisation, individualised medicine AMS subject classification: 92-02, 92B05 Biological common knowledge on cancerThis section shortly presents the general scenery of cancer evolution and features that must be included in models designed to describe and control it, bearing in mind a more descriptive (physicist's) than a therapeutic (physician's) point of view, only to reverse this perspective in the following sections, in which will be stressed the interest of modelling from the point of view of control, at least if one wants to design models for therapeutic applications. This biological section will be only a short sketch, if one considers that on this subject many books have already been written, e.g. [24,78,96,97,223]. Cancer: a challenging public health problemCardiovascular diseases and cancer are by fa...

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Circadian rhythms and protein turnover: The effect of temperature on the period lengths of clock mutants simulated by the Goodwin oscillator

Cited by 47 publications

References 29 publications

Circadian period lengths of lipid synthesis mutants (cel,chol-1) ofNeurosporashow defective temperature, but intact pH-compensation

Circadian period lengths of lipid synthesis mutants (cel,chol-1) ofNeurosporashow defective temperature, but intact pH-compensation

Protein sequestration versus Hill‐type repression in circadian clock models

Modelling Physiological and Pharmacological Control on Cell Proliferation to Optimise Cancer Treatments

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