Mammalian Skeletal Muscle Fiber Type Transitions

Pette, Dirk; Staron, Robert S.

doi:10.1016/s0074-7696(08)61622-8

Cited by 560 publications

(525 citation statements)

References 530 publications

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“…Development of slow characteristics is dependent on innervation by slow motor neurons, whereas development of fast characteristics is much less dependent on neural input (674). Expression of the fast phenotype is, however, co-regulated by thyroid hormone (671,674).…”

Section: [J4] Skeletal Musclementioning

confidence: 99%

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Bianco

Anderson

Forrest

et al. 2014

Thyroid

174

106

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Section: [J4] Skeletal Musclementioning

confidence: 99%

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Bianco

Anderson

Forrest

et al. 2014

Thyroid

174

106

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“…Additional, muscle-cell-extrinsic, mechanisms also contribute to fiber type differentiation. During normal development, some primary fibers transform from slow to fast and some secondary fibers transform from fast to slow (Condon et al, 1990a), and in adult life, fiber type can be experimentally transformed by changes in muscle usage patterns or in thyroid hormone levels (Pette and Staron, 1997).…”

Section: Introductionmentioning

confidence: 99%

TnIfast IRE enhancer: Multistep developmental regulation during skeletal muscle fiber type differentiation

Hallauer

Hastings

2002

Developmental Dynamics

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To identify developmental steps leading to adult skeletal muscle fiber-type-specific gene expression, we carried out transgenic mouse studies of the IRE enhancer of the quail TnIfast gene. Histochemical analysis of IRE/herpesvirus tk promoter/␤-galactosidase reporter transgene expression in adult muscle directly demonstrated IRE-driven fast vs. slow fiber-type specificity, and IIB>IIX>IIA differential expression among the fast fiber types: patterns similar to those of native-promoter TnIfast constructs. These tissue-and cell-type specificities are autonomous to the IRE and do not depend on interactions with a muscle gene promoter. Developmental studies showed that the adult pattern of IRE-driven transgene expression emerges in three steps: (1) activation during the formation of primary embryonic (presumptive slow) muscle fibers; (2) activation, to markedly higher levels, during formation of secondary (presumptive fast) fibers, and (3) differential augmentation of expression during early postnatal maturation of the IIB, IIX, IIA fast fiber types. These results provide insight into the roles of gene activation and gene repression mechanisms in fiber-type specificity and can account for apparently disparate results obtained in previous studies of TnI isoform expression in development. Each of the three IRE-driven developmental steps is spatiotemporally associated with a different major regulatory event at the fast myosin heavy chain gene cluster, suggesting that diverse muscle gene families respond to common, or tightly integrated, regulatory signals during multiple steps of muscle fiber differentiation.

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“…The functional, biochemical, and morphological differences between fiber types are a consequence of different fiber-specific gene expression patterns. Fibers are characterized by a remarkable plasticity and can be modulated by chronic low frequency electrical stimulation depending on the imposed activity pattern (2). Physiologically, this transformation process in fiber type occurs in response to altered demands, such as increases in muscle activity (3).…”

mentioning

confidence: 99%

The p38α/β Mitogen-activated Protein Kinases Mediate Recruitment of CREB-binding Protein to Preserve Fast Myosin Heavy Chain IId/x Gene Activity in Myotubes

Meißner¹,

Chang

Kubis³

et al. 2007

Journal of Biological Chemistry

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In skeletal muscle, the transformation of fast into slow fiber type is accompanied by shifts in fiber type-specific gene expression that includes down-regulation of the adult fast fiber myosin heavy chain IId/x (MyHCIId/x) gene. Here, we report that the mitogen-activated protein kinases (MAPKs) p38␣/␤ regulate MyHCIId/x gene expression. Electrical stimulation of rabbit skeletal muscle cells with a slow fiber type activity pattern and treatment of C2C12 myotubes with Ca 2؉ -ionophore inhibited p38␣/␤ MAPKs and reduced fast fiber type MyHC protein expression and promoter activity. Pharmacological inhibition of p38␣/␤ also down-regulated MyHCII gene expression. In controls, binding of the myocyte enhancer factor-2 (MEF-2) isoforms C and D as a heterodimer to a proximal consensus site within the MyHCIId/x promoter and recruitment of a transcriptional coactivator, the CREB-binding protein CBP, were observed. Overexpression of wild type MEF-2C but not of a MEF-2C mutant that cannot be phosphorylated by p38 induced promoter activity. Mutation of the MEF-2-binding site decreased the inducing effect of overexpressed CBP. Inhibition of p38␣/␤ MAPKs abolished CBP binding, whereas enforced induction of p38 by activated MAPK kinase 6 (MKK6EE) enhanced binding of CBP and increased promoter activity. Furthermore, knockdown of endogenous CBP by RNA interference eliminated promoter activation by MEF-2C or MKK6EE. In electrical stimulated and Ca 2؉ -ionophore-treated myotubes, CBP was absent in complex formation at that site. Taken together, the data indicate that p38␣/␤ MAPKs-mediated coactivator recruitment at a proximal MEF-2 site is important for MyHCIId/x gene regulation in skeletal muscle.Skeletal muscle fibers have been classified into fiber types based on their contraction speed, force development, fatigability, and metabolic functions (1). The characteristic fiber types are fast twitch glycolytic (type IID/X and IIB), fast twitch oxidative/glycolytic (type IIA), and slow twitch oxidative (type I/␤). Fast fibers express the IID/X, IIB, or IIA isoform of the myosin heavy chain (MyHC), 3 whereas slow fibers predominantly express the type I/␤ isoform. The functional, biochemical, and morphological differences between fiber types are a consequence of different fiber-specific gene expression patterns. Fibers are characterized by a remarkable plasticity and can be modulated by chronic low frequency electrical stimulation depending on the imposed activity pattern (2). Physiologically, this transformation process in fiber type occurs in response to altered demands, such as increases in muscle activity (3). Fiber type shifts are also observed during aging and disease. The importance of changes in intracellular Ca 2ϩ as a trigger for fiber type transformation has clearly been demonstrated by a Ca 2ϩ -ionophore-induced fast-to-slow transformation in primary skeletal muscle cells (4, 5). The involvement of calcineurin, a Ca 2ϩ -calmodulin-regulated serine/threonine phosphatase, in transducing the Ca 2ϩ -signal into altered gene expre...

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Mammalian Skeletal Muscle Fiber Type Transitions

Cited by 560 publications

References 530 publications

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

TnIfast IRE enhancer: Multistep developmental regulation during skeletal muscle fiber type differentiation

The p38α/β Mitogen-activated Protein Kinases Mediate Recruitment of CREB-binding Protein to Preserve Fast Myosin Heavy Chain IId/x Gene Activity in Myotubes

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