Comprehensive Physiology Wiley Online Library

Emergence of Specialization in Skeletal Muscle

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Abstract

The sections in this article are:

1 Muscle Histogenesis
2 Peripheral Nerve Development
3 Myofiber Specialization
4 Contractile Proteins
4.1 Myosin
4.2 Tropomyosin and Troponin
Figure 1. Figure 1.

Rat intercostal muscle, 16 days of gestation, with large extracellular space. A, B, and C: 3 small primary‐generation myotubes aggregated in a group, their membranes intimately apposed. Gap junctions are commonly found interconnecting these cells at this stage of development. In the surrounding tissue there are several undifferentiated cells. × 10,000.

Figure 2. Figure 2.

Rat hindlimb, 19‐day fetus. A: 3 gap junctions (GJ) may be recognized as arrays of particles on A face of plasmalemma. × 21,000. Upper inscribed area and B, rudimentary myofibril observed in the limited area of cleaved cytoplasm. Characteristic 400‐Å hexagonal array of thick filaments and faint hexagonal array of thin filaments (circle) are partially obscured by very low, local shadowing angle, × 68,000. C: portion of 1 gap junction, lower inscribed area of A, is enlarged to reveal 8‐ to 9‐nm subunit particles in cluster configuration. × 81,000. N1 and N2, multinuclei. [From Rash and Staehelin 141.]

Figure 3. Figure 3.

Rat intercostal muscle, 18 days of gestation. Large primary‐generation myotubes, containing much glycogen and peripherally dispersed myofibrils, dominate cell groups. Undifferentiated cells and small secondary‐generation myotubes are intimately applied to their walls. Each muscle cell group is peripherally ensheathed by a basement membrane, × 6,000.

Figure 4. Figure 4.

Rat intercostal muscle, 18 days of gestation. Small secondary‐generation myotube lies in a shallow depression of the wall of a large primary myotube. Processes protrude from the secondary cell into invaginations of the wall of the large myotube; invaginations are probably developing T tubules. Intercellular space between cells measures 80–100 Å. The presence of these complex membrane relations implies coordinate function of the 2 cells. × 30,000. [From Kelly and Zacks 99.]

Figure 5. Figure 5.

Rat intercostal muscle at birth. Myofibers, packed with myofibrils, compose a muscle bundle. Myofibers vary greatly in size and intermingle in a checkerboard pattern. Small myofibers are interpreted to be secondary‐generation cells that have developed on the walls of large primary cells. A, satellite cell abuts wall of large myofiber. × 6,000. [From Kelly and Zacks 99.]

Figure 6. Figure 6.

Neural control of muscle cell formation in the rat embryo. Open hexagons, number of muscle units in aneural muscles from rat embryos injected with β‐bungarotoxin on day 14 and examined at later times. Filled circles, muscle unit formation in control animals (mean ± SD). [From Harris 71.]

Figure 7. Figure 7.

Rat intercostal muscle, 18 days of gestation. Large primary‐generation myotube containing much glycogen is surrounded by new generations of secondary cells. Arrow, group of axon sprouts approaching large myotube membrane. In this area of contact primary cell membranes have increased electron density, indicating early differentiation of postsynaptic membrane. This configuration suggests that the primary‐secondary cell complex is innervated as a single unit. [From Kelly and Zacks 100.]

Figure 8. Figure 8.

Motor units and muscle cell development in the rat lumbrical muscle. Number of muscle fibers plotted as a function of number of remaining motor units in muscles 4–5 wk old that had been partially or completely denervated at birth. Point at 12 motor units is from control muscles. Points, mean ± SD. [From Betz et al. 16.]

Figure 9. Figure 9.

Possible sequence of events leading to muscle fiber diversity. Light area, appreciable reaction of cells only with AF; dotted area, significant reaction with both AF and AS; dark area, appreciable reaction only with AS. A: group of primary‐generation fibers, surrounded by replicating mononucleated myoblasts, are being innervated by a pathfinder motoneuron (solid line). B: small, secondary‐generation cells have formed and are attached to primary cell walls. Successive cohorts of motoneurons (broken lines) are constrained to innervate the primary cell at the neuromuscular junction determined by the pathfinder motoneuron. Separate innervation of secondary cells is unusual at this time. Primary cells stain heavily with antibody to slow as well as to fast myosin; secondary cells stain heavily only with AF. C: secondary cells have relinquished their intimate connections with primary cells and have become independently innervated; their innervation is apparently derived from the multiple innervation of primary cells. At this point a major difference between developing fast and slow muscles is seen. While practically all secondary cells in fast muscle mature as type II fibers, most secondary soleus cells slowly convert to type I fibers during the 1st yr after birth 25. Generation of type I fibers from secondary cells postpartum may depend on the pattern of muscle usage, whereas initial formation of type I fibers from primary cells may have a different cause. [From Rubinstein and Kelly 153.]

Figure 10. Figure 10.

Schematic diagrams illustrating postnatal development of rat lumbrical muscle. A: at birth all muscle fibers are polyneuronally innervated. B: during the first 10 days postpartum motoneurons lose some of their terminals (dotted lines) through synapse elimination, but the same motoneurons form new synapses on newly produced muscle fibers (dashed lines). New muscle fibers probably become polyneuronally innervated. Synapse elimination and synapse formation balance one another so that there is little change in the number of synapses made by each motoneuron, and thus motor unit size remains approximately constant. C: between 10 and 20 days postpartum muscle fiber production ceases, but elimination of synapses from polyneuronally innervated fibers (dotted line) continues. Average motor unit size decreases. D: at about 20 days postpartum, adult pattern of innervation is reached, where each muscle fiber is singly innervated. [From Betz et al. 15.]

Figure 11. Figure 11.

Time relations of isometric twitch contractions of extensor digitorum longus (EDL) and soleus muscles at various times during development. Representative records of tension: time curves of isometric twitch contractions of EDL and soleus shown in A and B, respectively. Age of animal indicated in vertical column (left). C and D: times for contraction and half relaxation for EDL (filled circles) and soleus (open circles) plotted against animal age. Points above a on abscissas for muscles from animals aged 140 days or more. Arrows on graphs in C and D indicate mean values for contraction and half‐relaxation times of soleus (upper arrows) and EDL (lower arrows) from newborn animals. [From Close 41.]

Figure 12. Figure 12.

Serial transverse sections through calf muscles of 19‐day fetal rat hindlimb. FIB, fibula; TIB, tibia. Sections are stained by the indirect peroxidase‐antiperoxidase method with antibodies specific to adult fast (A) and adult slow (B) myosin. By this method positively stained fibers are dark. All fibers in the soleus (SOL) and extensor digitorum longus (EDL) react positively with antifast myosin, probably reflecting cross‐reactivity with an embryonic form of myosin. With antislow myosin almost all soleus fibers stain well, but in EDL only a select population of fibers stain well. They are arranged in a nonrandom fashion through the muscle, and their distribution simulates that of slow fibers in the more mature EDL.

Figure 13. Figure 13.

Rat EDL, 2 days postpartum. Serial, transverse sections stained by direct fluorescence with AF (antifast myosin; A) and AS (antislow myosin; B). Positively stained fibers are light. Almost all fibers stain well with AF, although a few, widely distributed fibers stain weakly. The latter stain intensely with AS and are thus interpreted to be developing slow fibers.

Figure 14. Figure 14.

Rat EDL, 14 days postpartum. Serial, transverse sections stained by direct fluorescence with AF (A) and AS (B). Adult pattern of myosin staining has been approached. Most but not all fibers are positive with AF; those that do not react with AF now react with AS.

Figure 15. Figure 15.

Rat EDL, 18 days of gestation. Serial, transverse sections stained by the peroxidase‐antiperoxidase (PAP) method with AF (A) and AS (B). Muscle primordium is composed mainly of large primary‐generation myotubes, most of which stain well with both AF and AS. Arrows, a few secondary‐generation cells attached to the walls of primary myotubes. All of these react strongly with AF and weakly with AS. [From Rubinstein and Kelly 153.]

Figure 16. Figure 16.

Rat soleus, 18 days of gestion. Serial, transverse sections stained by the PAP method with AF (A) and AS (B). All primary‐ and secondary‐generation fibers react strongly with AF. Unlike EDL, most soleus fibers are primary cells; there are very few secondary cells. Like EDL, however, most primary fibers additionally react with AS, whereas few of the secondary fibers bind this antibody well. Arrow, secondary cells reacting strongly with AF but weakly with AS. [From Rubinstein and Kelly 153.]

Figure 17. Figure 17.

Rat soleus, 2 days postpartum. Serial, transverse sections stained with AF (A) and AS (B) by direct fluorescence. By this stage most soleus fibers react weakly with AF but continue to stain well with AS. A number of smaller secondary‐generation fibers are seen closely apposed to larger fibers. These stain well with AF but weakly with AS.

Figure 18. Figure 18.

Rat soleus, 14 days postpartum. Serial, transverse sections stained with AF (A) and AS (B) by direct fluorescence. Fifty percent of the fibers react intensely with AF and not at all with AS. These are usually comparatively small and are interpreted to be secondary‐generation cells. The other 50% react well with AS and not with AF. These are the larger cells of the muscle and are interpreted to be primary‐generation, slow fibers.

Figure 19. Figure 19.

Coelectrophoresis of embryonic and adult myosin samples in 12.5% Polyacrylamide gels. A: myosins from embryonic chicken muscle (15 fig) and adult fast‐twitch muscle (15 μg). B: myosins from embronic chicken muscle (20 μg) and adult slow tonic muscle (30 μg). C: embryonic chicken twitch muscle myosin (30 μg). [From Sréter et al. 168.]

Figure 20. Figure 20.

Time course of developmental changes of the 3 fast light chains in chicken breast muscle. [From Roy et al. 149.]

Figure 21. Figure 21.

Two‐dimensional electrophoresis of EDL and soleus myosin light chains at different ages. A‐C: EDL myosin light chains at 19 days in utero, 2 days postpartum, and adult age, respectively. D‐F: soleus myosin light chains at 19 days in utero, 2 days postpartum, and adult age, respectively. Fast myosin light chains represented as follows: LC1F = 1f, LC2F = 2f, LC3F = 3f. Slow myosin light chains are LC1S = 1s, LC2S = 2s. [From Rubinstein and Kelly 152.]

Figure 22. Figure 22.

Solid lines, standard developmental time courses (contraction time‐age curves) for slow and fast muscles in the cat. Broken lines, postulated time course for these muscles in the absence of suprasegmental neural influences. [From Buller et al. 29.]

Figure 23. Figure 23.

Myosin isozyme profiles from normal slow‐twitch soleus (N‐SOL) and normal fast‐twitch EDL (N‐EDL) muscles of the rat. Electrophoresis with 4% Polyacrylamide gels was performed for 9 h at 80 V and in 20 mM sodium pryophosphate buffer (pH 8.8, with 10% glycerol). Gels were stained in Coomassie blue and scanned at 550 nm. A: profile from each muscle superimposed. B: results of coelectrophoresis. Numbers indicate different types of myosin isozymes. [From Hoh et al. 77.]

Figure 24. Figure 24.

Myosin isozyme profiles of EDL and soleus muscles of normal and cordotomized rat. A: superimposed myosin isozyme profiles for EDL from normal (N‐EDL, solid line) and cordotomized (T‐EDL, broken line) rats. B: superimposed myosin isozyme profiles for soleus from normal (N‐SOL) and cordotomized (T‐SOL) rats. Muscles from cordotomized rat, 8 wk postoperatively, and from normal rat of same age. [From Hoh et al. 77.]

Figure 25. Figure 25.

Analysis of embryonic, newborn, and adult tissue myofibrils. Muscle tissue was dissected from 20‐day‐old rat embryos and was glycerinated. Soleus muscle was dissected from newborn rats of 3, 7, and 12 days as well as from an adult, and these were glycerinated. Crude myofibrils were analyzed by 2‐dimensional gel electrophoresis. A: 20‐day embryonic muscle (120 μl). B: 3‐day soleus (100 μl). C: 7‐day soleus (120 μl). D: 12‐day soleus (100 μl). E: adult soleus (30 μl). Vertical arrows, embryonic light‐chain LC1 protein. The 2 additional spots in A correspond to LC1F and LC2F. The 2 spots in E correspond to LC1S and LC2S. In B‐D there are mixtures of fast and slow light chains. [From Whalen et al. 186.]

Figure 26. Figure 26.

Two‐dimensional gel electrophoretic analysis of chymotryptic myosin cleavage products. Myosins from bulk tissue (A), soleus (B), cardiac tissue (C), 20‐day embryonic bulk (D), L6 cultures (E), and primary cultures (F). Primary culture myosin degraded in the presence of nonradioactive L6 myosin. Approximately 15,000 count/min loaded in F. Gels are presented with samples in the basic pH range to the left and decreasing molecular weight from top to bottom. Excess chymotrypsin added to gel in C; its position is indicated (Ch). Corresponding Ch spot can be seen in all stained gels (A‐E). This 2‐dimensional analysis demonstrates that soleus and cardiac myosin degradation patterns are closely related but can be distinguished by some of the polypeptides present (see arrows in Figs. 3B, C). Myosin from embryonic tissue, primary cultures, and L6 cells have very similar cleavage patterns, but these patterns are different from those of adult myosins. [From Whalen et al. 188.]

Figure 27. Figure 27.

Relative proportions of tropomyosin subunits α (white area) and β (hatched area) in various striated muscles of chicken and rabbit. ALD, anterior latissimus dorsi; PLD, posterior latissimus dorsi. [From Roy et al. 149.]



Figure 1.

Rat intercostal muscle, 16 days of gestation, with large extracellular space. A, B, and C: 3 small primary‐generation myotubes aggregated in a group, their membranes intimately apposed. Gap junctions are commonly found interconnecting these cells at this stage of development. In the surrounding tissue there are several undifferentiated cells. × 10,000.



Figure 2.

Rat hindlimb, 19‐day fetus. A: 3 gap junctions (GJ) may be recognized as arrays of particles on A face of plasmalemma. × 21,000. Upper inscribed area and B, rudimentary myofibril observed in the limited area of cleaved cytoplasm. Characteristic 400‐Å hexagonal array of thick filaments and faint hexagonal array of thin filaments (circle) are partially obscured by very low, local shadowing angle, × 68,000. C: portion of 1 gap junction, lower inscribed area of A, is enlarged to reveal 8‐ to 9‐nm subunit particles in cluster configuration. × 81,000. N1 and N2, multinuclei. [From Rash and Staehelin 141.]



Figure 3.

Rat intercostal muscle, 18 days of gestation. Large primary‐generation myotubes, containing much glycogen and peripherally dispersed myofibrils, dominate cell groups. Undifferentiated cells and small secondary‐generation myotubes are intimately applied to their walls. Each muscle cell group is peripherally ensheathed by a basement membrane, × 6,000.



Figure 4.

Rat intercostal muscle, 18 days of gestation. Small secondary‐generation myotube lies in a shallow depression of the wall of a large primary myotube. Processes protrude from the secondary cell into invaginations of the wall of the large myotube; invaginations are probably developing T tubules. Intercellular space between cells measures 80–100 Å. The presence of these complex membrane relations implies coordinate function of the 2 cells. × 30,000. [From Kelly and Zacks 99.]



Figure 5.

Rat intercostal muscle at birth. Myofibers, packed with myofibrils, compose a muscle bundle. Myofibers vary greatly in size and intermingle in a checkerboard pattern. Small myofibers are interpreted to be secondary‐generation cells that have developed on the walls of large primary cells. A, satellite cell abuts wall of large myofiber. × 6,000. [From Kelly and Zacks 99.]



Figure 6.

Neural control of muscle cell formation in the rat embryo. Open hexagons, number of muscle units in aneural muscles from rat embryos injected with β‐bungarotoxin on day 14 and examined at later times. Filled circles, muscle unit formation in control animals (mean ± SD). [From Harris 71.]



Figure 7.

Rat intercostal muscle, 18 days of gestation. Large primary‐generation myotube containing much glycogen is surrounded by new generations of secondary cells. Arrow, group of axon sprouts approaching large myotube membrane. In this area of contact primary cell membranes have increased electron density, indicating early differentiation of postsynaptic membrane. This configuration suggests that the primary‐secondary cell complex is innervated as a single unit. [From Kelly and Zacks 100.]



Figure 8.

Motor units and muscle cell development in the rat lumbrical muscle. Number of muscle fibers plotted as a function of number of remaining motor units in muscles 4–5 wk old that had been partially or completely denervated at birth. Point at 12 motor units is from control muscles. Points, mean ± SD. [From Betz et al. 16.]



Figure 9.

Possible sequence of events leading to muscle fiber diversity. Light area, appreciable reaction of cells only with AF; dotted area, significant reaction with both AF and AS; dark area, appreciable reaction only with AS. A: group of primary‐generation fibers, surrounded by replicating mononucleated myoblasts, are being innervated by a pathfinder motoneuron (solid line). B: small, secondary‐generation cells have formed and are attached to primary cell walls. Successive cohorts of motoneurons (broken lines) are constrained to innervate the primary cell at the neuromuscular junction determined by the pathfinder motoneuron. Separate innervation of secondary cells is unusual at this time. Primary cells stain heavily with antibody to slow as well as to fast myosin; secondary cells stain heavily only with AF. C: secondary cells have relinquished their intimate connections with primary cells and have become independently innervated; their innervation is apparently derived from the multiple innervation of primary cells. At this point a major difference between developing fast and slow muscles is seen. While practically all secondary cells in fast muscle mature as type II fibers, most secondary soleus cells slowly convert to type I fibers during the 1st yr after birth 25. Generation of type I fibers from secondary cells postpartum may depend on the pattern of muscle usage, whereas initial formation of type I fibers from primary cells may have a different cause. [From Rubinstein and Kelly 153.]



Figure 10.

Schematic diagrams illustrating postnatal development of rat lumbrical muscle. A: at birth all muscle fibers are polyneuronally innervated. B: during the first 10 days postpartum motoneurons lose some of their terminals (dotted lines) through synapse elimination, but the same motoneurons form new synapses on newly produced muscle fibers (dashed lines). New muscle fibers probably become polyneuronally innervated. Synapse elimination and synapse formation balance one another so that there is little change in the number of synapses made by each motoneuron, and thus motor unit size remains approximately constant. C: between 10 and 20 days postpartum muscle fiber production ceases, but elimination of synapses from polyneuronally innervated fibers (dotted line) continues. Average motor unit size decreases. D: at about 20 days postpartum, adult pattern of innervation is reached, where each muscle fiber is singly innervated. [From Betz et al. 15.]



Figure 11.

Time relations of isometric twitch contractions of extensor digitorum longus (EDL) and soleus muscles at various times during development. Representative records of tension: time curves of isometric twitch contractions of EDL and soleus shown in A and B, respectively. Age of animal indicated in vertical column (left). C and D: times for contraction and half relaxation for EDL (filled circles) and soleus (open circles) plotted against animal age. Points above a on abscissas for muscles from animals aged 140 days or more. Arrows on graphs in C and D indicate mean values for contraction and half‐relaxation times of soleus (upper arrows) and EDL (lower arrows) from newborn animals. [From Close 41.]



Figure 12.

Serial transverse sections through calf muscles of 19‐day fetal rat hindlimb. FIB, fibula; TIB, tibia. Sections are stained by the indirect peroxidase‐antiperoxidase method with antibodies specific to adult fast (A) and adult slow (B) myosin. By this method positively stained fibers are dark. All fibers in the soleus (SOL) and extensor digitorum longus (EDL) react positively with antifast myosin, probably reflecting cross‐reactivity with an embryonic form of myosin. With antislow myosin almost all soleus fibers stain well, but in EDL only a select population of fibers stain well. They are arranged in a nonrandom fashion through the muscle, and their distribution simulates that of slow fibers in the more mature EDL.



Figure 13.

Rat EDL, 2 days postpartum. Serial, transverse sections stained by direct fluorescence with AF (antifast myosin; A) and AS (antislow myosin; B). Positively stained fibers are light. Almost all fibers stain well with AF, although a few, widely distributed fibers stain weakly. The latter stain intensely with AS and are thus interpreted to be developing slow fibers.



Figure 14.

Rat EDL, 14 days postpartum. Serial, transverse sections stained by direct fluorescence with AF (A) and AS (B). Adult pattern of myosin staining has been approached. Most but not all fibers are positive with AF; those that do not react with AF now react with AS.



Figure 15.

Rat EDL, 18 days of gestation. Serial, transverse sections stained by the peroxidase‐antiperoxidase (PAP) method with AF (A) and AS (B). Muscle primordium is composed mainly of large primary‐generation myotubes, most of which stain well with both AF and AS. Arrows, a few secondary‐generation cells attached to the walls of primary myotubes. All of these react strongly with AF and weakly with AS. [From Rubinstein and Kelly 153.]



Figure 16.

Rat soleus, 18 days of gestion. Serial, transverse sections stained by the PAP method with AF (A) and AS (B). All primary‐ and secondary‐generation fibers react strongly with AF. Unlike EDL, most soleus fibers are primary cells; there are very few secondary cells. Like EDL, however, most primary fibers additionally react with AS, whereas few of the secondary fibers bind this antibody well. Arrow, secondary cells reacting strongly with AF but weakly with AS. [From Rubinstein and Kelly 153.]



Figure 17.

Rat soleus, 2 days postpartum. Serial, transverse sections stained with AF (A) and AS (B) by direct fluorescence. By this stage most soleus fibers react weakly with AF but continue to stain well with AS. A number of smaller secondary‐generation fibers are seen closely apposed to larger fibers. These stain well with AF but weakly with AS.



Figure 18.

Rat soleus, 14 days postpartum. Serial, transverse sections stained with AF (A) and AS (B) by direct fluorescence. Fifty percent of the fibers react intensely with AF and not at all with AS. These are usually comparatively small and are interpreted to be secondary‐generation cells. The other 50% react well with AS and not with AF. These are the larger cells of the muscle and are interpreted to be primary‐generation, slow fibers.



Figure 19.

Coelectrophoresis of embryonic and adult myosin samples in 12.5% Polyacrylamide gels. A: myosins from embryonic chicken muscle (15 fig) and adult fast‐twitch muscle (15 μg). B: myosins from embronic chicken muscle (20 μg) and adult slow tonic muscle (30 μg). C: embryonic chicken twitch muscle myosin (30 μg). [From Sréter et al. 168.]



Figure 20.

Time course of developmental changes of the 3 fast light chains in chicken breast muscle. [From Roy et al. 149.]



Figure 21.

Two‐dimensional electrophoresis of EDL and soleus myosin light chains at different ages. A‐C: EDL myosin light chains at 19 days in utero, 2 days postpartum, and adult age, respectively. D‐F: soleus myosin light chains at 19 days in utero, 2 days postpartum, and adult age, respectively. Fast myosin light chains represented as follows: LC1F = 1f, LC2F = 2f, LC3F = 3f. Slow myosin light chains are LC1S = 1s, LC2S = 2s. [From Rubinstein and Kelly 152.]



Figure 22.

Solid lines, standard developmental time courses (contraction time‐age curves) for slow and fast muscles in the cat. Broken lines, postulated time course for these muscles in the absence of suprasegmental neural influences. [From Buller et al. 29.]



Figure 23.

Myosin isozyme profiles from normal slow‐twitch soleus (N‐SOL) and normal fast‐twitch EDL (N‐EDL) muscles of the rat. Electrophoresis with 4% Polyacrylamide gels was performed for 9 h at 80 V and in 20 mM sodium pryophosphate buffer (pH 8.8, with 10% glycerol). Gels were stained in Coomassie blue and scanned at 550 nm. A: profile from each muscle superimposed. B: results of coelectrophoresis. Numbers indicate different types of myosin isozymes. [From Hoh et al. 77.]



Figure 24.

Myosin isozyme profiles of EDL and soleus muscles of normal and cordotomized rat. A: superimposed myosin isozyme profiles for EDL from normal (N‐EDL, solid line) and cordotomized (T‐EDL, broken line) rats. B: superimposed myosin isozyme profiles for soleus from normal (N‐SOL) and cordotomized (T‐SOL) rats. Muscles from cordotomized rat, 8 wk postoperatively, and from normal rat of same age. [From Hoh et al. 77.]



Figure 25.

Analysis of embryonic, newborn, and adult tissue myofibrils. Muscle tissue was dissected from 20‐day‐old rat embryos and was glycerinated. Soleus muscle was dissected from newborn rats of 3, 7, and 12 days as well as from an adult, and these were glycerinated. Crude myofibrils were analyzed by 2‐dimensional gel electrophoresis. A: 20‐day embryonic muscle (120 μl). B: 3‐day soleus (100 μl). C: 7‐day soleus (120 μl). D: 12‐day soleus (100 μl). E: adult soleus (30 μl). Vertical arrows, embryonic light‐chain LC1 protein. The 2 additional spots in A correspond to LC1F and LC2F. The 2 spots in E correspond to LC1S and LC2S. In B‐D there are mixtures of fast and slow light chains. [From Whalen et al. 186.]



Figure 26.

Two‐dimensional gel electrophoretic analysis of chymotryptic myosin cleavage products. Myosins from bulk tissue (A), soleus (B), cardiac tissue (C), 20‐day embryonic bulk (D), L6 cultures (E), and primary cultures (F). Primary culture myosin degraded in the presence of nonradioactive L6 myosin. Approximately 15,000 count/min loaded in F. Gels are presented with samples in the basic pH range to the left and decreasing molecular weight from top to bottom. Excess chymotrypsin added to gel in C; its position is indicated (Ch). Corresponding Ch spot can be seen in all stained gels (A‐E). This 2‐dimensional analysis demonstrates that soleus and cardiac myosin degradation patterns are closely related but can be distinguished by some of the polypeptides present (see arrows in Figs. 3B, C). Myosin from embryonic tissue, primary cultures, and L6 cells have very similar cleavage patterns, but these patterns are different from those of adult myosins. [From Whalen et al. 188.]



Figure 27.

Relative proportions of tropomyosin subunits α (white area) and β (hatched area) in various striated muscles of chicken and rabbit. ALD, anterior latissimus dorsi; PLD, posterior latissimus dorsi. [From Roy et al. 149.]

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How to Cite

Alan M. Kelly. Emergence of Specialization in Skeletal Muscle. Compr Physiol 2011, Supplement 27: Handbook of Physiology, Skeletal Muscle: 507-537. First published in print 1983. doi: 10.1002/cphy.cp100117