Multilaminar aggregates of sarcoplasmic reticulum in caudal muscle cells of an ascidian larva

1980 ◽  
Vol 58 (4) ◽  
pp. 538-542
Author(s):  
Michael J. Cavey
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Muscle Cells ◽  
Ascidian Larva ◽  
The Cross

The sarcoplasmic reticulum (SR) in caudal muscle cells of the larva of the polycitorid ascidian Distaplia occidentalis consists of perifibrillar cisternae and coextensive cisternal aggregates. The multilaminar aggregates resemble the interdigitated collars of perifibrillar SR which embrace the sarcomeric H-bands of the cross-striated myofibrils. Cisternae of the coextensive sarcoplasmic reticulum neither envelop the contractile myofilaments nor couple to the sarcolemma. Ultra-structural evidence is suggestive that the coextensive multilaminar aggregates are transient elements of the sarcoplasmic reticulum.

Ultrastructure of the caudal muscle cells in the larva of a polyclinid ascidian

1985 ◽  
Vol 63 (6) ◽  
pp. 1410-1419 ◽  
Author(s):  
Michael J. Cavey ◽  
Harvey D. Strecker
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Striated Muscle ◽  
Muscle Cells ◽  
The Other ◽  
The Cross

Two paraxial bands of somatic striated muscle occur in the tail of the larva of the compound ascidian Aplidium ?constellatum. The mononucleate muscle cells of each band align in longitudinal rows between the epidermis and the notochord. The cross-striated myofibrils, originating and terminating at intermediate junctions on the transverse cellular boundaries, are indiscrete. They follow a spiral course through the subcortical and medullary sarcoplasm, bypassing the nucleus and the other organelles and inclusions in the center of the cell. Cisternae of the sarcoplasmic reticulum envelop the myofibrils, forming compact fenestrated sheets that are continuous between the sarcomeres and locally undifferentiated with respect to the myofibrillar striations. Cisternae of the perifibrillar sarcoplasmic reticulum near each sarcomeric Z-line establish dyadic interior couplings with a network of tubular invaginations of the sarcolemma. The sarcolemmal tubules can originate from any surface, including the transverse cellular boundaries. Near the half I-bands of the terminal sarcomeres at the intermediate junctions, the perifibrillar cisternae frequently leave the fenestrated sheets and extend to the overlying sarcolemma, becoming the sub-sarcolemmal cisternae of dyadic peripheral couplings.

Removal of dystroglycan causes severe muscular dystrophy in zebrafish embryos

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3505-3512 ◽  
Author(s):  
Michael J. Parsons ◽  
Isabel Campos ◽  
Elizabeth M. A. Hirst ◽  
Derek L. Stemple
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Muscular Dystrophy ◽  
Muscle Cells ◽  
Laminin Receptor ◽  
Central Component ◽  
Zebrafish Embryos ◽  
Term Survival ◽  
Α Subunit ◽  
Glycoprotein Complex ◽  
Dystrophin Glycoprotein Complex

Muscular dystrophy is frequently caused by disruption of the dystrophin-glycoprotein complex (DGC), which links muscle cells to the extracellular matrix. Dystroglycan, a central component of the DGC, serves as a laminin receptor via its extracellular α subunit, and interacts with dystrophin (and thus the actin cytoskeleton) through its integral membrane β subunit. We have removed the function of dystroglycan in zebrafish embryos. In contrast to mouse, where dystroglycan mutations lead to peri-implantation lethality, dystroglycan is dispensable for basement membrane formation during early zebrafish development. At later stages, however, loss of dystroglycan leads to a disruption of the DGC, concurrent with loss of muscle integrity and necrosis. In addition, we find that loss of the DGC leads to loss of sarcomere and sarcoplasmic reticulum organisation. The DGC is required for long-term survival of muscle cells in zebrafish, but is dispensable for muscle formation. Dystroglycan or the DGC is also required for normal sarcomere and sarcoplasmic reticulum organisation. Because zebrafish embryos lacking dystroglycan share several characteristics with human muscular dystrophy, they should serve as a useful model for the disease. In addition, knowing the dystroglycan null phenotype in zebrafish will facilitate the isolation of other molecules involved in muscular dystrophy pathogenesis.

Effect of isosmotic removal of extracellular Ca2+ and of membrane potential on cell volume in muscle cells

1994 ◽  
Vol 267 (3) ◽  
pp. C768-C775 ◽  
Author(s):  
C. Pena-Rasgado ◽  
K. D. McGruder ◽  
J. C. Summers ◽  
H. Rasgado-Flores
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Cell Volume ◽  
Muscle Cells ◽  
Membrane Depolarization ◽  
Volume Reduction ◽  
Sensitive Volume ◽  
Volume Increase ◽  
Dependent Cell ◽  
In Cells

Isosmotic removal of extracellular Ca2+ (Cao) and changes in membrane potential (Vm) are frequently performed manipulations. Using isolated voltage-clamped barnacle muscle cells, we studied the effect of these manipulations on isosmotic cell volume. Replacing Cao by Mg2+ induced 1) verapamil-sensitive extracellular Na(+)-dependent membrane depolarization, 2) membrane depolarization-dependent cell volume reduction in cells whose sarcoplasmic reticulum (SR) was presumably loaded with Ca2+ [intracellular Ca2+ (Cai)-loaded cells], and 3) cell volume increase in cells whose SR was presumably depleted of Ca2+ (Cai-depleted cells) or in Cai-loaded cells whose Vm was held constant. Membrane depolarization induced 1) volume reduction in Cai-loaded cells or 2) verapamil-sensitive volume increase in Cai-depleted cells. This suggests tha, in Cai-loaded cells, membrane depolarization induces SR Ca2+ release, which in turn promotes volume reduction. Conversely, in Cai-depleted cells, the depolarization activates Na+ influx through a verapamil-sensitive pathway leading to the volume increase. This pathway is also revealed when Cao is removed in either Cai-depleted cells or in cells whose Vm is held constant.

Stored calcium modulates inositol phosphate synthesis in cultured smooth muscle cells

1992 ◽  
Vol 263 (2) ◽  
pp. C535-C539 ◽  
Author(s):  
D. M. Berman ◽  
W. F. Goldman
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Smooth Muscle Cells ◽  
Inverse Relationship ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
A7r5 Cells ◽  
Cultured Smooth Muscle Cells

Cytosolic Ca2+ concentrations ([Ca2+]cyt) and [3H]inositol phosphates ([3H]InsP) were correlated while varying the Ca2+ content of the sarcoplasmic reticulum (SR) in cultured A7r5 cells at rest and during activation with [Arg8]-vasopressin (AVP). Thapsigargin (TG) raised and superfusion with 0 Ca2+ lowered [Ca2+]cyt, but both treatments decreased SR Ca2+ and AVP-evoked Ca2+ transients. Neither TG nor 0 Ca2+ affected basal [3H]InsP, but both treatments increased AVP-evoked synthesis of [3H]InsP. Exposure for several minutes to 40 mM K+ solution, BAY K 8644, or low-Na+ solution all elevated [Ca2+]cyt and, thereby, increased SR Ca2+, as manifested by augmented AVP-evoked Ca2+ transients. In all three cases, AVP-evoked, but not basal, [3H]InsP were reduced. The inhibitory effect of 40 mM K+ on AVP-evoked [3H]InsP synthesis was blocked when SR Ca2+ uptake was prevented by TG. Brief (30-s) exposures to 40 mM K+, which elevated [Ca2+]cyt but not SR Ca2+ loading, did not modify AVP-evoked [3H]InsP synthesis or Ca2+ transients. These results demonstrate an inverse relationship between SR Ca2+ content and evoked [3H]-InsP synthesis. Moreover, they suggest that SR Ca2+ may serve as a signal that modulates sarcolemmal [3H]InsP formation.

scholarly journals DIFFERENTIATION OF THE SARCOPLASMIC RETICULUM AND T SYSTEM IN DEVELOPING CHICK SKELETAL MUSCLE IN VITRO

1967 ◽  
Vol 35 (2) ◽  
pp. 405-420 ◽  
Author(s):  
Elizabeth B. Ezerman ◽  
Harunori Ishikawa
Keyword(s):  
Skeletal Muscle ◽  
Electron Microscope ◽  
Sarcoplasmic Reticulum ◽  
Osmium Tetroxide ◽  
Muscle Cells ◽  
Simultaneous Occurrence ◽  
Chick Embryos ◽  
Developing Muscle ◽  
T System

The electron microscope was used to investigate the first 10 days of differentiation of the SR and the T system in skeletal muscle cultured from the breast muscle of 11-day chick embryos. The T-system tubules could be clearly distinguished from the SR in developing muscle cells fixed with glutaraldehyde and osmium tetroxide. Ferritin diffusion confirmed this finding: the ferritin particles were found only in the tubules identified as T system. The proliferation of both membranous systems seemed to start almost simultaneously at the earliest myotube stage. Observations suggested that the new SR membranes developed from the rough-surfaced ER as tubular projections. The SR tubules connected with one another to form a network around the myofibril. The T-system tubules were formed by invagination of the sarcolemma. The early extension of the T system by branching and budding was seen only in subsarcolemmal regions. Subsequently the T-system tubules could be seen deep within the muscle cells. Immediately after invaginating, the T-system tubule formed, along its course, specialized connections with the SR or ER: triadic structures showing various degrees of differentiation. The simultaneous occurrence of myofibril formation and membrane proliferation is considered to be important in understanding the coordinated events resulting in the differentiated myotube.

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