scholarly journals Synchronization, oscillator death, and frequency modulation in a class of biologically inspired coupled oscillators

Author(s):  
Alessio Franci ◽  
Marco A Herrera-Valdez ◽  
Miguel Lara-Aparicio ◽  
Pablo Padilla-Longoria

The general purpose of this paper is to build up on our understanding of the basic mathematical principles that underlie the emergence of synchronous biological rhythms, in particular, the circadian clock. To do so, we study the role that the coupling strength, coupling type, and noise play in the synchronization of a system of coupled, nonlinear oscillators. First, we study a deterministic model based on Van der Pol coupled oscillators, modeling a population of diffusively coupled cells, to find regions in the parameter space for which synchronous oscillations emerge and to provide conditions under which diffusive coupling kills the synchronous oscillation. Second, we study how noise and coupling interact and lead to synchronous oscillations in linearly coupled oscillators, modeling the interaction between various pacemaker populations, each having an endogenous circadian clock. To do so, we use the Fokker-Planck equation associated to the system. We show how coupling can tune the frequency of the emergent synchronous oscillation, which provides a general mechanism to make fast (ultradian) pacemakers slow (circadian) and synchronous via coupling. The basic mechanisms behind the generation of oscillations and the emergence of synchrony that we describe here can be used to guide further studies of coupled oscillations in biophysical nonlinear models.

2018 ◽  
Author(s):  
Alessio Franci ◽  
Marco A Herrera-Valdez ◽  
Miguel Lara-Aparicio ◽  
Pablo Padilla-Longoria

The general purpose of this paper is to build up on our understanding of the basic mathematical principles that underlie the emergence of synchronous biological rhythms, in particular, the circadian clock. To do so, we study the role that the coupling strength, coupling type, and noise play in the synchronization of a system of coupled, nonlinear oscillators. First, we study a deterministic model based on Van der Pol coupled oscillators, modeling a population of diffusively coupled cells, to find regions in the parameter space for which synchronous oscillations emerge and to provide conditions under which diffusive coupling kills the synchronous oscillation. Second, we study how noise and coupling interact and lead to synchronous oscillations in linearly coupled oscillators, modeling the interaction between various pacemaker populations, each having an endogenous circadian clock. To do so, we use the Fokker-Planck equation associated to the system. We show how coupling can tune the frequency of the emergent synchronous oscillation, which provides a general mechanism to make fast (ultradian) pacemakers slow (circadian) and synchronous via coupling. The basic mechanisms behind the generation of oscillations and the emergence of synchrony that we describe here can be used to guide further studies of coupled oscillations in biophysical nonlinear models.


2018 ◽  
Author(s):  
Marco A Herrera-Valdez ◽  
Pablo Padilla-Longoria ◽  
Alessio Franci ◽  
Miguel Lara-Aparicio

The general purpose of this paper is to build up on our understanding of the basic mathematical principles that underlie the emergence of biological rhythms, in particular, the circadian clock. To do so, we study the role that the coupling strength and noise play in the synchronization of a system of nonlinear, linearly coupled oscillators. First, we study a deterministic version of the model to find plausible regions in the parameter space for which synchronization is observed. Second, we focus on studying how noise and coupling interact in determining the synchronized behavior. To do so, we leverage the Fokker-Planck equation associated with the system. The basic mechanisms behind the generation of oscillations and the emergence of synchrony that we describe here can be used as a guide to further study coupled oscillations in biophysical nonlinear models.


Author(s):  
S. Vadde ◽  
J. K. Allen ◽  
F. Mistree

Abstract Catalog design is a procedure in which a system is assembled by selecting standard components from catalogs of available components. Selection in design involves making a choice among a number of alternatives taking into account several attributes. The information available to a designer to do so during the early stages of project initiation may be uncertain. The uncertainty in information may be imprecise or stochastic. Under these circumstances, a designer has to balance limited resources against the quality of solution obtained or decisions made by accounting for uncertainty in information available. This complex task becomes formidable when dealing with coupled selection problems, that is problems that should be solved simultaneously. Coupled selection problems share a number of coupling attributes among them. In an earlier paper we have shown how selection problems, both coupled and uncoupled can be reformulated as a single compromise Decision Support Problem (DSP) using a deterministic model. In this paper, we show how the traditional compromise DSP can be extended to represent a nondeterministic case. We use fuzzy set theory to model imprecision and Bayesian statistics to model stochastic information. Formulations that can be solved with the same solution scheme are presented to handle both fuzzy and stochastic information in the standard framework of a compromise DSP. The approaches are illustrated by an example involving the coupled selection of a heat exchanger concept and a cooling fluid for a specific application. The emphasis in this paper is placed on explaining the methods.


2021 ◽  
Vol 251 (3356) ◽  
pp. 15
Author(s):  
Jason Arunn Murugesu

2020 ◽  
Author(s):  
Zihao Zhu ◽  
Marcel Quint ◽  
Muhammad Usman Anwer

SummaryPredictable changes in light and temperature during a diurnal cycle are major entrainment cues that enable the circadian clock to generate internal biological rhythms that are synchronized with the external environment. With the average global temperature predicted to keep increasing, the intricate light-temperature coordination that is necessary for clock functionality is expected to be seriously affected. Hence, understanding how temperature signals are perceived by the circadian clock has become an important issue, especially in light of climate change scenarios. In Arabidopsis, the clock component EARLY FLOWERING 3 (ELF3) not only serves as an essential light Zeitnehmer, but also functions as a thermosensor participating in thermomorphogenesis. However, the role of ELF3 in temperature entrainment of the circadian clock is not fully understood. Here, we report that ELF3 is essential for delivering temperature input to the clock. We demonstrate that in the absence of ELF3, the oscillator was unable to properly respond to temperature changes, resulting in an impaired gating of thermoresponses. Consequently, clock-controlled physiological processes such as rhythmic growth and cotyledon movement were disturbed. Together, our results reveal that ELF3 is an essential Zeitnehmer for temperature sensing of the oscillator, and thereby for coordinating the rhythmic control of thermoresponsive physiological outputs.


BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Kate A. Rawlinson ◽  
Adam J. Reid ◽  
Zhigang Lu ◽  
Patrick Driguez ◽  
Anna Wawer ◽  
...  

Abstract Background The consequences of the earth’s daily rotation have led to 24-h biological rhythms in most organisms. Even some parasites are known to have daily rhythms, which, when in synchrony with host rhythms, can optimise their fitness. Understanding these rhythms may enable the development of control strategies that take advantage of rhythmic vulnerabilities. Recent work on protozoan parasites has revealed 24-h rhythms in gene expression, drug sensitivity and the presence of an intrinsic circadian clock; however, similar studies on metazoan parasites are lacking. To address this, we investigated if a metazoan parasite has daily molecular oscillations, whether they reveal how these longer-lived organisms can survive host daily cycles over a lifespan of many years and if animal circadian clock genes are present and rhythmic. We addressed these questions using the human blood fluke Schistosoma mansoni that lives in the vasculature for decades and causes the tropical disease schistosomiasis. Results Using round-the-clock transcriptomics of male and female adult worms collected from experimentally infected mice, we discovered that ~ 2% of its genes followed a daily pattern of expression. Rhythmic processes included a stress response during the host’s active phase and a ‘peak in metabolic activity’ during the host’s resting phase. Transcriptional profiles in the female reproductive system were mirrored by daily patterns in egg laying (eggs are the main drivers of the host pathology). Genes cycling with the highest amplitudes include predicted drug targets and a vaccine candidate. These 24-h rhythms may be driven by host rhythms and/or generated by a circadian clock; however, orthologs of core clock genes are missing and secondary clock genes show no 24-h rhythmicity. Conclusions There are daily rhythms in the transcriptomes of adult S. mansoni, but they appear less pronounced than in other organisms. The rhythms reveal temporally compartmentalised internal processes and host interactions relevant to within-host survival and between-host transmission. Our findings suggest that if these daily rhythms are generated by an intrinsic circadian clock then the oscillatory mechanism must be distinct from that in other animals. We have shown which transcripts oscillate at this temporal scale and this will benefit the development and delivery of treatments against schistosomiasis.


1977 ◽  
Vol 70 (1) ◽  
pp. 167-181
Author(s):  
JACK A. BENSON ◽  
JON W. JACKLET

1. The circadian clock that controls CAP frequency was stopped at or near its lowest phase point by long duration cold pulses of 6 °C. On return to normal recording temperature (15 °C), the rhythm was always reinitiated from this phase point. 2. Following long cold pulses, there was often a transient peak of CAP activity lasting 2-6 h. It is thought that this was an effect of rise in temperature after prolonged cooling and not an effect on the clock itself. 3. Twelve h cold pulses, spanning the rhythm peak, caused phase delays. 9 °C pulses caused small delays (e.g. 1.7 h) while large phase delays (e.g. 6.7 h) followed pulses of 5 °C. Some pulses at an intermediate temperature (8.5 °C) caused abnormal post-pulse cycles lasting several days, and resulting in very large phase delays (10–14 n). 4. The abnormal CAP frequency curves following 12 h cold pulses of 8.5 °C spanning the rhythm peak are interpreted as rhythm splits. It is postulated that part of the population of coupled oscillators comprising the circadian clock was slightly delayed by the cold pulse, while the other part was driven further towards the “stopped” state, thus producing a large phase angle difference between the two subpopulations. These drew one another back into phase during several cycles to reform a normal circadian rhythm. 5. It is hypothesized that the circadian oscillations of the two subpopulations did not sum to produce the observed CAP frequency curve; rather the level of CAP output was controlled by whichever subpopulation was discharging at the higher frequency. Note: Laboratory of Sensory Sciences, University of Hawaii at Manoa, 1993 East-West Road, Honolulu, Hawaii 96822, U.S.A.


2014 ◽  
Vol 4 (3) ◽  
pp. 20130076 ◽  
Author(s):  
Daniel DeWoskin ◽  
Weihua Geng ◽  
Adam R. Stinchcombe ◽  
Daniel B. Forger

Biological rhythms, generated by feedback loops containing interacting genes, proteins and/or cells, time physiological processes in many organisms. While many of the components of the systems that generate biological rhythms have been identified, much less is known about the details of their interactions. Using examples from the circadian (daily) clock in three organisms, Neurospora , Drosophila and mouse, we show, with mathematical models of varying complexity, how interactions among (i) promoter sites, (ii) proteins forming complexes, and (iii) cells can have a drastic effect on timekeeping. Inspired by the identification of many transcription factors, for example as involved in the Neurospora circadian clock, that can both activate and repress, we show how these multiple actions can cause complex oscillatory patterns in a transcription–translation feedback loop (TTFL). Inspired by the timekeeping complex formed by the NMO–PER–TIM–SGG complex that regulates the negative TTFL in the Drosophila circadian clock, we show how the mechanism of complex formation can determine the prevalence of oscillations in a TTFL. Finally, we note that most mathematical models of intracellular clocks model a single cell, but compare with experimental data from collections of cells. We find that refitting the most detailed model of the mammalian circadian clock, so that the coupling between cells matches experimental data, yields different dynamics and makes an interesting prediction that also matches experimental data: individual cells are bistable, and network coupling removes this bistability and causes the network to be more robust to external perturbations. Taken together, we propose that the interactions between components in biological timekeeping systems are carefully tuned towards proper function. We also show how timekeeping can be controlled by novel mechanisms at different levels of organization.


2019 ◽  
Vol 34 (4) ◽  
pp. 380-390 ◽  
Author(s):  
Young M. Jeong ◽  
Cristiano Dias ◽  
Casey Diekman ◽  
Helene Brochon ◽  
Pyonghwa Kim ◽  
...  

The circadian clock controls 24-h biological rhythms in our body, influencing many time-related activities such as sleep and wake. The simplest circadian clock is found in cyanobacteria, with the proteins KaiA, KaiB, and KaiC generating a self-sustained circadian oscillation of KaiC phosphorylation and dephosphorylation. KaiA activates KaiC phosphorylation by binding the A-loop of KaiC, while KaiB attenuates the phosphorylation by sequestering KaiA from the A-loop. Structural analysis revealed that magnesium regulates the phosphorylation and dephosphorylation of KaiC by dissociating from and associating with catalytic Glu residues that activate phosphorylation and dephosphorylation, respectively. High magnesium causes KaiC to dephosphorylate, whereas low magnesium causes KaiC to phosphorylate. KaiC alone behaves as an hourglass timekeeper when the magnesium concentration is alternated between low and high levels in vitro. We suggest that a magnesium-based hourglass timekeeping system may have been used by ancient cyanobacteria before magnesium homeostasis was established.


2013 ◽  
Vol 280 (1765) ◽  
pp. 20130433 ◽  
Author(s):  
Roelof A. Hut ◽  
Silvia Paolucci ◽  
Roi Dor ◽  
Charalambos P. Kyriacou ◽  
Serge Daan

Properties of the circadian and annual timing systems are expected to vary systematically with latitude on the basis of different annual light and temperature patterns at higher latitudes, creating specific selection pressures. We review literature with respect to latitudinal clines in circadian phenotypes as well as in polymorphisms of circadian clock genes and their possible association with annual timing. The use of latitudinal (and altitudinal) clines in identifying selective forces acting on biological rhythms is discussed, and we evaluate how these studies can reveal novel molecular and physiological components of these rhythms.


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