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      Microtubule Organization in Striated Muscle Cells

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          Abstract

          Distinctly organized microtubule networks contribute to the function of differentiated cell types such as neurons, epithelial cells, skeletal myotubes, and cardiomyocytes. In striated (i.e., skeletal and cardiac) muscle cells, the nuclear envelope acts as the dominant microtubule-organizing center (MTOC) and the function of the centrosome—the canonical MTOC of mammalian cells—is attenuated, a common feature of differentiated cell types. We summarize the mechanisms known to underlie MTOC formation at the nuclear envelope, discuss the significance of the nuclear envelope MTOC for muscle function and cell cycle progression, and outline potential mechanisms of centrosome attenuation.

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          Skeletal muscle: a brief review of structure and function.

          Skeletal muscle is one of the most dynamic and plastic tissues of the human body. In humans, skeletal muscle comprises approximately 40% of total body weight and contains 50-75% of all body proteins. In general, muscle mass depends on the balance between protein synthesis and degradation and both processes are sensitive to factors such as nutritional status, hormonal balance, physical activity/exercise, and injury or disease, among others. In this review, we discuss the various domains of muscle structure and function including its cytoskeletal architecture, excitation-contraction coupling, energy metabolism, and force and power generation. We will limit the discussion to human skeletal muscle and emphasize recent scientific literature on single muscle fibers.
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            The oxygen-rich postnatal environment induces cardiomyocyte cell-cycle arrest through DNA damage response.

            The mammalian heart has a remarkable regenerative capacity for a short period of time after birth, after which the majority of cardiomyocytes permanently exit cell cycle. We sought to determine the primary postnatal event that results in cardiomyocyte cell-cycle arrest. We hypothesized that transition to the oxygen-rich postnatal environment is the upstream signal that results in cell-cycle arrest of cardiomyocytes. Here, we show that reactive oxygen species (ROS), oxidative DNA damage, and DNA damage response (DDR) markers significantly increase in the heart during the first postnatal week. Intriguingly, postnatal hypoxemia, ROS scavenging, or inhibition of DDR all prolong the postnatal proliferative window of cardiomyocytes, whereas hyperoxemia and ROS generators shorten it. These findings uncover a protective mechanism that mediates cardiomyocyte cell-cycle arrest in exchange for utilization of oxygen-dependent aerobic metabolism. Reduction of mitochondrial-dependent oxidative stress should be an important component of cardiomyocyte proliferation-based therapeutic approaches. Copyright © 2014 Elsevier Inc. All rights reserved.
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              The cytoplasmic dynein transport machinery and its many cargoes

              Cytoplasmic dynein-1 is an important microtubule-based motor in many eukaryotic cells. Dynein has critical roles both in interphase and during cell division. Here we focus on interphase cargoes of dynein, which include membrane-bound organelles, RNAs, protein complexes and viruses. A central challenge in the field is to understand how a single motor can transport such a diverse array of cargoes and how this process is regulated. The molecular basis by which each cargo is linked to dynein and its cofactor dynactin has started to emerge. Of particular importance for this process is a set of coiled coil proteins — ‘activating adaptors’ — which both recruit dynein–dynactin to their cargoes and activate dynein motility.
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                Author and article information

                Journal
                Cells
                Cells
                cells
                Cells
                MDPI
                2073-4409
                03 June 2020
                June 2020
                : 9
                : 6
                : 1395
                Affiliations
                [1 ]Experimental Renal and Cardiovascular Research, Department of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany; robert.becker@ 123456uk-erlangen.de (R.B.); marina.leone@ 123456i-med.ac.at (M.L.)
                [2 ]Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria
                [3 ]Muscle Research Center Erlangen (MURCE), 91054 Erlangen, Germany
                Author notes
                Author information
                https://orcid.org/0000-0003-2605-3429
                Article
                cells-09-01395
                10.3390/cells9061395
                7349303
                32503326
                4fb782d5-505a-4519-936f-0c2a8f934497
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 30 April 2020
                : 28 May 2020
                Categories
                Review

                centrosome,mtoc,non-centrosomal mtoc,skeletal muscle,cardiomyocytes,cell cycle,microtubules

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