scholarly journals The myogenic electric organ ofSternopygus macrurus: a non-contractile tissue with a skeletal muscle transcriptome

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e1828 ◽  
Author(s):  
Matthew Pinch ◽  
Robert Güth ◽  
Manoj P. Samanta ◽  
Alexander Chaidez ◽  
Graciela A. Unguez
Keyword(s):  
Skeletal Muscle ◽  
Striated Muscle ◽  
Electric Organ ◽  
Cell Types ◽  
Sarcomeric Proteins ◽  
Muscle Properties ◽  
Functional Studies ◽  
Myogenic Program ◽  
Contractile Tissue ◽  
Skeletal Muscle Transcriptome

In most electric fish species, the electric organ (EO) derives from striated muscle cells that suppress many muscle properties. In the gymnotiformSternopygus macrurus, mature electrocytes, the current-producing cells of the EO, do not contain sarcomeres, yet they continue to make some cytoskeletal and sarcomeric proteins and the muscle transcription factors (MTFs) that induce their expression. In order to more comprehensively examine the transcriptional regulation of genes associated with the formation and maintenance of the contractile sarcomere complex, results from expression analysis using qRT-PCR were informed by deep RNA sequencing of transcriptomes and miRNA compositions of muscle and EO tissues from adultS. macrurus. Our data show that: (1) components associated with the homeostasis of the sarcomere and sarcomere-sarcolemma linkage were transcribed in EO at levels similar to those in muscle; (2) MTF families associated with activation of the skeletal muscle program were not differentially expressed between these tissues; and (3) a set of microRNAs that are implicated in regulation of the muscle phenotype are enriched in EO. These data support the development of a unique and highly specialized non-contractile electrogenic cell that emerges from a striated phenotype and further differentiates with little modification in its transcript composition. This comprehensive analysis of parallel mRNA and miRNA profiles is not only a foundation for functional studies aimed at identifying mechanisms underlying the transcription-independent myogenic program inS. macrurusEO, but also has important implications to many vertebrate cell types that independently activate or suppress specific features of the skeletal muscle program.

scholarly journals Triadin Binding to the C-Terminal Luminal Loop of the Ryanodine Receptor is Important for Skeletal Muscle Excitation–Contraction Coupling

2007 ◽  
Vol 130 (4) ◽  
pp. 365-378 ◽  
Author(s):  
Sanjeewa A. Goonasekera ◽  
Nicole A. Beard ◽  
Linda Groom ◽  
Takashi Kimura ◽  
Alla D. Lyfenko ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ryanodine Receptor ◽  
Calcium Release ◽  
Striated Muscle ◽  
Single Channel ◽  
Triple Mutant ◽  
Double Mutation ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Functional Studies

Ca2+ release from intracellular stores is controlled by complex interactions between multiple proteins. Triadin is a transmembrane glycoprotein of the junctional sarcoplasmic reticulum of striated muscle that interacts with both calsequestrin and the type 1 ryanodine receptor (RyR1) to communicate changes in luminal Ca2+ to the release machinery. However, the potential impact of the triadin association with RyR1 in skeletal muscle excitation–contraction coupling remains elusive. Here we show that triadin binding to RyR1 is critically important for rapid Ca2+ release during excitation–contraction coupling. To assess the functional impact of the triadin-RyR1 interaction, we expressed RyR1 mutants in which one or more of three negatively charged residues (D4878, D4907, and E4908) in the terminal RyR1 intraluminal loop were mutated to alanines in RyR1-null (dyspedic) myotubes. Coimmunoprecipitation revealed that triadin, but not junctin, binding to RyR1 was abolished in the triple (D4878A/D4907A/E4908A) mutant and one of the double (D4907A/E4908A) mutants, partially reduced in the D4878A/D4907A double mutant, but not affected by either individual (D4878A, D4907A, E4908A) mutations or the D4878A/E4908A double mutation. Functional studies revealed that the rate of voltage- and ligand-gated SR Ca2+ release were reduced in proportion to the degree of interruption in triadin binding. Ryanodine binding, single channel recording, and calcium release experiments conducted on WT and triple mutant channels in the absence of triadin demonstrated that the luminal loop mutations do not directly alter RyR1 function. These findings demonstrate that junctin and triadin bind to different sites on RyR1 and that triadin plays an important role in ensuring rapid Ca2+ release during excitation–contraction coupling in skeletal muscle.

scholarly journals Current Strategies for the Regeneration of Skeletal Muscle Tissue

2021 ◽  
Vol 22 (11) ◽  
pp. 5929
Author(s):  
Emine Alarcin ◽  
Ayca Bal-Öztürk ◽  
Hüseyin Avci ◽  
Hamed Ghorbanpoor ◽  
Fatma Dogan Guzel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Muscle Regeneration ◽  
Striated Muscle ◽  
Cell Types ◽  
Skeletal Muscle Tissue ◽  
Skeletal Muscle Regeneration ◽  
Muscle Repair ◽  
Clinical Implementation ◽  
Different Cell Types

Traumatic injuries, tumor resections, and degenerative diseases can damage skeletal muscle and lead to functional impairment and severe disability. Skeletal muscle regeneration is a complex process that depends on various cell types, signaling molecules, architectural cues, and physicochemical properties to be successful. To promote muscle repair and regeneration, various strategies for skeletal muscle tissue engineering have been developed in the last decades. However, there is still a high demand for the development of new methods and materials that promote skeletal muscle repair and functional regeneration to bring approaches closer to therapies in the clinic that structurally and functionally repair muscle. The combination of stem cells, biomaterials, and biomolecules is used to induce skeletal muscle regeneration. In this review, we provide an overview of different cell types used to treat skeletal muscle injury, highlight current strategies in biomaterial-based approaches, the importance of topography for the successful creation of functional striated muscle fibers, and discuss novel methods for muscle regeneration and challenges for their future clinical implementation.

scholarly journals Gene regulatory networks and cell lineages that underlie the formation of skeletal muscle

2017 ◽  
Vol 114 (23) ◽  
pp. 5830-5837 ◽  
Author(s):  
Margaret Buckingham
Keyword(s):  
Skeletal Muscle ◽  
Gene Regulatory Networks ◽  
Regulatory Networks ◽  
Striated Muscle ◽  
Neck Muscles ◽  
Trunk Muscles ◽  
T Box ◽  
Lineage Tree ◽  
Gene Regulatory ◽  
Myogenic Program

Skeletal muscle in vertebrates is formed by two major routes, as illustrated by the mouse embryo. Somites give rise to myogenic progenitors that form all of the muscles of the trunk and limbs. The behavior of these cells and their entry into the myogenic program is controlled by gene regulatory networks, where paired box gene 3 (Pax3) plays a predominant role. Head and some neck muscles do not derive from somites, but mainly form from mesoderm in the pharyngeal region. Entry into the myogenic program also depends on the myogenic determination factor (MyoD) family of genes, but Pax3 is not expressed in these myogenic progenitors, where different gene regulatory networks function, with T-box factor 1 (Tbx1) and paired-like homeodomain factor 2 (Pitx2) as key upstream genes. The regulatory genes that underlie the formation of these muscles are also important players in cardiogenesis, expressed in the second heart field, which is a major source of myocardium and of the pharyngeal arch mesoderm that gives rise to skeletal muscles. The demonstration that both types of striated muscle derive from common progenitors comes from clonal analyses that have established a lineage tree for parts of the myocardium and different head and neck muscles. Evolutionary conservation of the two routes to skeletal muscle in vertebrates extends to chordates, to trunk muscles in the cephlochordate Amphioxus and to muscles derived from cardiopharyngeal mesoderm in the urochordate Ciona, where a related gene regulatory network determines cardiac or skeletal muscle cell fates. In conclusion, Eric Davidson’s visionary contribution to our understanding of gene regulatory networks and their evolution is acknowledged.

scholarly journals Cilia, Centrosomes and Skeletal Muscle

2021 ◽  
Vol 22 (17) ◽  
pp. 9605
Author(s):  
Dominic C. H. Ng ◽  
Uda Y. Ho ◽  
Miranda D. Grounds
Keyword(s):  
Cell Cycle ◽  
Skeletal Muscle ◽  
Cell Fate ◽  
Developmental Disorders ◽  
Cell Cycle Progression ◽  
Primary Cilia ◽  
Striated Muscle ◽  
Cell Types ◽  
Extracellular Milieu ◽  
A Cell

Primary cilia are non-motile, cell cycle-associated organelles that can be found on most vertebrate cell types. Comprised of microtubule bundles organised into an axoneme and anchored by a mature centriole or basal body, primary cilia are dynamic signalling platforms that are intimately involved in cellular responses to their extracellular milieu. Defects in ciliogenesis or dysfunction in cilia signalling underlie a host of developmental disorders collectively referred to as ciliopathies, reinforcing important roles for cilia in human health. Whilst primary cilia have long been recognised to be present in striated muscle, their role in muscle is not well understood. However, recent studies indicate important contributions, particularly in skeletal muscle, that have to date remained underappreciated. Here, we explore recent revelations that the sensory and signalling functions of cilia on muscle progenitors regulate cell cycle progression, trigger differentiation and maintain a commitment to myogenesis. Cilia disassembly is initiated during myoblast fusion. However, the remnants of primary cilia persist in multi-nucleated myotubes, and we discuss their potential role in late-stage differentiation and myofiber formation. Reciprocal interactions between cilia and the extracellular matrix (ECM) microenvironment described for other tissues may also inform on parallel interactions in skeletal muscle. We also discuss emerging evidence that cilia on fibroblasts/fibro–adipogenic progenitors and myofibroblasts may influence cell fate in both a cell autonomous and non-autonomous manner with critical consequences for skeletal muscle ageing and repair in response to injury and disease. This review addresses the enigmatic but emerging role of primary cilia in satellite cells in myoblasts and myofibers during myogenesis, as well as the wider tissue microenvironment required for skeletal muscle formation and homeostasis.

Assembly Of Myofibrils in Vertebrate Cross-Striated Muscle Cells

2000 ◽  
Vol 6 (S2) ◽  
pp. 78-79
Author(s):  
J. W. Sanger ◽  
J. M. Sanger
Keyword(s):  
Skeletal Muscle ◽  
Fluorescent Protein ◽  
Striated Muscle ◽  
Myosin Ii ◽  
Cardiac Cells ◽  
Chick Embryos ◽  
Sarcomeric Proteins ◽  
Different Types ◽  
Green Fluorescent ◽  
Muscle Myosin

This presentation will review how myofibrils are formed in both types of vertebrate cross-striated myofibrils, i.e., cardiac and skeletal muscle.Cardiomyocytes isolated from 7 to 9 day-old chick embryos and myoblasts isolated from 10-day old quail embryos were placed in tissue culture. The cardiac cells were allowed to spread in culture for 3 - 5 days. Similarly, the myoblasts were permitted to fuse to form myotubes which were then fixed at different points of elongation over 3 -5 days. Some cultures were fixed and stained with antibodies (e.g., sarcomeric isoform of alpha-actinin; non-muscle myosin IIB and muscle myosin II) to detect the disposition of the forming and mature myofibrils inside these cells. Sister cultures were transfected with plasmids expressing Green Fluorescent Protein (GFP) ligated sarcomeric proteins like alpha-actinin. The staining and transfection results revealed that three different types of fibrils form during myofibrillogenesis: premyofibrils, nascent myofibrils and mature myofibrils (1-2).

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