The physical imperative in circadian rhythm: a cytoskeleton-related physically resettable clock mechanism hypothesis

Shweiki, Dorit

doi:10.1054/mehy.1998.0785

Cited by 9 publications

(3 citation statements)

References 70 publications

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“…In fact, the tensegrity principle could explain pattern formation in various tissues and organs in species ranging from mammals (Ingber and Jamieson, 1985;Joshi et al, 1985;Van Essen, 1997;GalliResta, 2002) to paramecium (Kaczanowska et al, 1995) and fungi (Kaminsky and Heath, 1996), as well as loss of tissue morphology during cancer formation (Ingber et al, 1981;Ingber and Jamieson, 1985;. It also may provide a molecular basis for gravity sensing (Ingber, 1999;Yoder et al, 2001) and control of circadian rhythmicity (Shweiki, 1999) in both animals and plants. In addition, tensegrity may help to explain why cellular components that are not directly involved in actomyosin-based tension generation, such as microtubules, intermediate filaments and ECM, can contribute significantly to contractile function in various cell types, including cardiac myocytes, vascular smooth muscle and skeletal muscle (Northover and Northover, 1993;Tsutsui et al, 1993;Lee et al, 1997;Tagawa et al, 1997;D'Angelo et al, 1997;Eckes et al, 1998;Gillis, 1999;Wang and Stamenovic, 2000;Keller et al, 2001;Balogh et al, 2002;Loufrani et al, 2002) as well as to control of permeability barrier function in endothelia (Moy et al, 1998).…”

Section: Tissue Morphogenesis In Contextmentioning

confidence: 99%

Tensegrity II. How structural networks influence cellular information processing networks

Ingber

2003

Journal of Cell Science

747

467

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IntroductionBiology and medicine are currently undergoing a paradigm shift. Up until now, we have focused on identifying the molecular components that comprise life, with the hope that rigorous characterization of all the parts will lead to understanding of the whole. As a result of sequencing the genomes of multiple organisms, including the human, it is now clear that there is more to the equation: the whole is truly greater than the sum of its parts. Thus, biology is shifting away from reductionism and towards the development of methods and approaches necessary to deal with 'biocomplexity'. The challenge is to understand how complex cell and tissue behaviors emerge from collective interactions among multiple molecular components at the genomic and proteomic levels and to describe molecular processes as integrated, hierarchical systems rather than isolated parts.Another driving force behind this paradigm shift is the resurgence of interest in mechanical forces, rather than chemicals cues, as biological regulators. Clinicians have come to recognize the importance of mechanical forces for the development and function of the heart and lung, the growth of skin and muscle, the maintenance of cartilage and bone, and the etiology of many debilitating diseases, including hypertension, osteoporosis, asthma and heart failure. Exploration of basic physiological mechanisms, such as sound sensation, motion recognition and gravity detection, has also demanded explanation in mechanical terms. At the same time, the introduction of new techniques for manipulating and probing individual molecules and cells has revealed the

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Section: Tissue Morphogenesis In Contextmentioning

confidence: 99%

Tensegrity II. How structural networks influence cellular information processing networks

Ingber

2003

Journal of Cell Science

747

467

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“…Maintenance of circadian rhythms requires exquisite synaptic coordination at multiple molecular and cellular levels of brain organization. The emergence of this complex circadian clock network requires both stable and dynamic properties of the neuronal cytoskeleton (Shweiki, 1999). Microtubules are key components of the cytoskeleton and their localization, mass, and dynamics are very important in many intracellular processes in neuronal health and disease (Brandt and Bakota, 2017; Dent, 2017).…”

Section: Introductionmentioning

confidence: 99%

Role of Tau Protein in Remodeling of Circadian Neuronal Circuits and Sleep

Arnés

Alaniz

Karam

et al. 2019

Front. Aging Neurosci.

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Multiple neurological, physiological, and behavioral functions are synchronized by circadian clocks into daily rhythms. Neurodegenerative diseases such as Alzheimer’s disease and related tauopathies are associated with a decay of circadian rhythms, disruption of sleep patterns, and impaired cognitive function but the mechanisms underlying these alterations are still unclear. Traditional approaches in neurodegeneration research have focused on understanding how pathology impinges on circadian function. Since in Alzheimer’s disease and related tauopathies tau proteostasis is compromised, here we sought to understand the role of tau protein in neuronal circadian biology and related behavior. Considering molecular mechanisms underlying circadian rhythms are conserved from Drosophila to humans, here we took advantage of a recently developed tau-deficient Drosophila line to show that loss of tau promotes dysregulation of daily circadian rhythms and sleep patterns. Strikingly, tau deficiency dysregulates the structural plasticity of the small ventral lateral circadian pacemaker neurons by disrupting the temporal cytoskeletal remodeling of its dorsal axonal projections and by inducing a slight increase in the cytoplasmic accumulation of core clock proteins. Taken together, these results suggest that loss of tau function participates in the regulation of circadian rhythms by modulating the correct operation and connectivity of core circadian networks and related behavior.

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“…The presence of Clock within the myofilaments could enable the protein to "sense" cross-bridge cycling in myocytes, a major source of energy expenditure. Some have theorized that the circadian system in cells could operate through mechanotransduction in association with the cytoskeleton [20]. In myocytes, mechanosensing may play an important role in the regulation of the internal circadian clock.…”

Section: Discussionmentioning

confidence: 99%

The circadian protein Clock localizes to the sarcomeric Z-disk and is a sensor of myofilament cross-bridge activity in cardiac myocytes

Qi¹,

Boateng²

2006

Biochemical and Biophysical Research Communications

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In the mammalian heart, the circadian protein Clock regulates glucose and fatty acid metabolism. In this study, we determined some of the factors that regulate Clock expression and subcellular distribution in myocytes. Using immunochemistry and biochemical subcellular fractionation, we have shown that Clock localizes to the Z-disk of the myofilaments. Increasing calcium and crossbridge cycling with 10μM phenylephrine for 48 hours resulted in a 3 fold increase in Clock and a translocation of the protein to the nucleus. When myofilament cross-bridge cycling was inhibited with 10 μM verapamil or 7.5 mM butanedione monoxime for 48 hours, both significantly reduced the presence of Clock in the nucleus and cytoskeleton. These results suggest that the expression and subcellular distribution of Clock can be altered by changes in cross-bridge cycling, a major source of energy expenditure in myocytes. We suggest that the circadian Clock protein may help coordinate the sensing of energy expenditure with energy supply.

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The physical imperative in circadian rhythm: a cytoskeleton-related physically resettable clock mechanism hypothesis

Cited by 9 publications

References 70 publications

Tensegrity II. How structural networks influence cellular information processing networks

Tensegrity II. How structural networks influence cellular information processing networks

Role of Tau Protein in Remodeling of Circadian Neuronal Circuits and Sleep

The circadian protein Clock localizes to the sarcomeric Z-disk and is a sensor of myofilament cross-bridge activity in cardiac myocytes

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