What Is the Basic Unit of Contraction in a Muscle Cell
Skeletal muscle is made up of cells collectively called muscle fibers. Each muscle fiber is multinucleated with its nuclei located along the periphery of the fiber. Each muscle fiber is further divided into myofibrils, which are the basic units of the muscle fiber. These myofibrils are surrounded by the muscular cell membrane (sarkolemma), which forms deep intussusceptions called transverse tubules (T-tubules) in the myofibrillus. Each myofibril contains contractile proteins, described as thick, thin filaments, arranged longitudinally in units called sarcomeres. miRNA-208a controls not only the expression of β-CMH in the heart, but also that of the closely related slow myosin isoform Myh7b (van Rooij et al., 2009). The genes β-CMH and Myh7b encode intronic miRNAs, miRNA-208b and miRNA-499, respectively (Berezikov et al., 2006; Landgraf et al., 2007). Mice lacking the miRNA-208b or miRNA-499 gene have no obvious developmental defects (van Rooij et al., 2009). However, miRNA-208b/-499 double zero mutated mice exhibit reduced expression of slow myofiber β-MHC and increased expression of fast-type myosin isoforms.
In contrast, overexpression of miRNA-499 leads to increased expression of β-MHC and leads muscles to a slow myofiber phenotype. Forced expression of cardiac miRNA-499 promotes hypertrophy in mice (Shieh et al., 2011; Matkovich et al., 2012). Together, these miRNAs are important for specifying muscle fiber identity by stimulating slow myofiber gene programs at the expense of those controlling the rapid expression of the myoffiber gene (Hodgkinson et al., 2015). miRNA-133a suppresses smooth muscle gene expression in the heart by directly targeting the myocardium and SRF for suppression (Liu et al., 2008; Wystub et al., 2013). Deletion of miRNA-133a-1 and mIRNA-133a-2 (miRNA-133a null) causes late embryonic and neonatal lethality due to ventricular septal abnormalities (VOD) and ventricular dilation (Liu et al., 2008). MiRNA-133a null mice show sarcomer disorganization and ectopic activation of the smooth muscle gene program (Liu et al., 2008). In addition, mice lacking both miRNA-1 and miRNA-133a exhibited severe cardiac dysfunction and died before embryonic day 11.5 (E11.5). Mice with a zero mutation in miRNA-1/133a showed increased expression of myocardial and smooth muscle genes in the heart. These studies suggest that the miRNA-1 and miRNA-133a groups are important for cardiomyocyte differentiation and sarcoma formation during embryonic and postnatal life. They work cooperatively to control the gene transition program from an immature state characterized by the expression of smooth muscle genes to a mature phenotype (Wystub et al., 2013). Hoyle, G. Comparative aspects of muscle.
Annual Review of Physiology 31, 43–82 (1969) doi:10.1146/annurev.ph.31.030169.000355. The expression of the isoforms α and β-CMH is controlled by miRNA-208a, miRNA-208b and miRNA-499 (van Rooij et al., 2007, 2009; Callis et al., 2009). miRNA-208a and miRNA-208b are encoded in an intron of the genes α-MHC and β-MHC, respectively. Zero mice for miRNA-208a are viable, but have abnormalities in sarcomer structure and decreased heart function at 6 months of age (van Rooij et al., 2007). However, zero miRNA-208a mice are resistant to cardiac hypertrophy in response to stress induced by transverse aortic ligament or calcineurin formation (van Rooij et al., 2007; Callis et al., 2009). This is accompanied by a decrease in the expression of the slow contractile skeletal muscle protein β-MHC in zero miRNA-208a cores. The function of miRNA-208a is mediated in part by the suppression of protein 1 associated with thyroid hormone receptors (Thrap1), which negatively regulates the expression of β-MHC. Skeletal muscle spasms are due to sudden and involuntary muscle contractions that last from a few seconds to a few minutes and lead to pain.
Although they can be associated with diseases, muscle spasms most often occur in the absence of a clear pathology. They most often occur in older patients, who are pregnant or exercise vigorously. Since cramps are the product of muscle contractions, immediate pain relief can be achieved by stretching the affected muscle.  Describe the structure and function of skeletal muscle fibers Each skeletal muscle fiber is supplied by a motor neuron to the NMJ. Watch this video to learn more about what happens at the neuromuscular connection. (a) What is the definition of a motor unit? (b) What is the structural and functional difference between a large motor unit and a small motor unit? Can you give an example for everyone? (c) Why is the neurotransmitter acetylcholine broken down after binding to its receptor? In skeletal muscle, which works with tendons to pull on bones, collagen in the three layers of connective tissue intertwines with collagen from a tendon. At the other end of the tendon, it merges with the periosteum that covers the bone. The tension created by the contraction of muscle fibers is then transferred through the layers of connective tissue to the tendon and then to the periosteum to pull on the bone for the movement of the skeleton. .