Innervation‐dependent and fiber type‐specific transcriptional regulation of the slow myosin heavy chain 2 promoter in avian skeletal muscle fibers

Jiang, Hongbin; Jordan, Theresa; Li, Jinyuan; Li, Hui; DiMario, Joseph X.

doi:10.1002/dvdy.20137

Cited by 23 publications

(52 citation statements)

References 62 publications

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“…During in vivo fetal muscle development, however, the local environment (extrinsic to muscle cells) plays a deciding role in modulating the final fiber types eventually displayed by the myotubes (Dunglison et al, 1999;Hughes, 1999;Robson and Hughes, 1999). Innervation is undoubtedly an important part of the extrinsic regulatory mechanism, which has been shown both in vivo (McLennan, 1994;Lefeuvre et al, 1996;Washabaugh et al, 1998), as well as in vitro using co-cultures of the nerve and myotubes (Jiang et al, 2004;Jordan et al, 2005). In addition, maturation and survival of both primary and secondary myotubes are largely dependent on innervation (Hughes and Ontell, 1992;Ashby et al, 1993a,b;Wilson and Harris, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…The role of Wnt signaling in fiber type differentiation of mammalian fetal skeletal muscle remains unknown. Although the innervation-dependent extrinsic signals that determine fetal muscle fiber types have started to be uncovered (Jiang et al, 2004;Jordan et al, 2003Jordan et al, , 2005, the intrinsic and innervationindependent extrinsic factors that regulate initial fiber types of fetal muscle have not been identified.…”

Section: Discussionmentioning

confidence: 99%

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Sox6 is required for normal fiber type differentiation of fetal skeletal muscle in mice

Hagiwara

Yeh

Liu

2007

Developmental Dynamics

140

138

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Sox6, a member of the Sox family of transcription factors, is highly expressed in skeletal muscle. Despite its abundant expression, the role of Sox6 in muscle development is not well understood. We hypothesize that, in fetal muscle, Sox6 functions as a repressor of slow fiber type-specific genes. In the wild-type mouse, differentiation of fast and slow fibers becomes apparent during late fetal stages (after approximately embryonic day 16). However, in the Sox6 null-p 100H mutant mouse, all fetal muscle fibers maintain slow fiber characteristics, as evidenced by expression of the slow myosin heavy chain MyHC-␤. Knockdown of Sox6 expression in wild-type myotubes results in a significant increase in MyHC-␤ expression, supporting our hypothesis. Analysis of the MyHC-␤ promoter revealed a Sox consensus sequence that likely functions as a negative cis-regulatory element. Together, our results suggest that Sox6 plays a critical role in the fiber type differentiation of fetal skeletal muscle.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sox6 is required for normal fiber type differentiation of fetal skeletal muscle in mice

Hagiwara

Yeh

Liu

2007

Developmental Dynamics

140

138

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“…A mutagenesis study (19) has indicated that both NFAT and MEF2 binding sites are required for innervation-induced MyHC2 promoter activity in slow muscle fibers. Basically, there is NFAT activation by RyR inhibition (20), whereas IP3R blockade results in the opposite effect (21).…”

Section: Discussionmentioning

confidence: 99%

NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells

Valdés¹,

Gaggero²,

Hidalgo³

et al. 2008

American Journal of Physiology-Cell Physiology

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. NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells. Am J Physiol Cell Physiol 294: C715-C725, 2008. First published January 9, 2008 doi:10.1152/ajpcell.00195.2007.-Depolarization of skeletal muscle cells triggers intracellular Ca 2ϩ signals mediated by ryanodine and inositol 1,4,5-trisphosphate (IP3) receptors. Previously, we have reported that K ϩ -induced depolarization activates transcriptional regulators ERK, cAMP response element-binding protein, c-fos, c-jun, and egr-1 through IP3-dependent Ca 2ϩ release, whereas NF-B activation is elicited by both ryanodine and IP3 receptor-mediated Ca 2ϩ signals. We have further shown that field stimulation with electrical pulses results in an NF-B activation increase dependent of the amount of pulses and independent of their frequency. In this work, we report the results obtained for nuclear factor of activated T cells (NFAT)-mediated transcription and translocation generated by both K ϩ and electrical stimulation protocols in primary skeletal muscle cells and C2C12 cells. The Ca 2ϩ source for NFAT activation is through release by ryanodine receptors and extracellular Ca 2ϩ entry. We found this activation to be independent of the number of pulses within a physiological range of stimulus frequency and enhanced by long-lasting low-frequency stimulation. Therefore, activation of the NFAT signaling pathway differs from that of NF-B and other transcription factors. Calcineurin enzyme activity correlated well with the relative activation of NFAT translocation and transcription using different stimulation protocols. Furthermore, both K ϩ -induced depolarization and electrical stimulation increased mRNA levels of the type 1 IP3 receptor mediated by calcineurin activity, which suggests that depolarization may regulate IP3 receptor transcription. These results confirm the presence of at least two independent pathways for excitationtranscription coupling in skeletal muscle cells, both dependent on Ca 2ϩ release and triggered by the same voltage sensor but activating different intracellular release channels. nuclear factor of activated T cells transcription; nuclear factor of activated T cells translocation; calcineurin; inositol 1,4,5-trisphosphate receptor; ryanodine receptor IN SKELETAL MUSCLE CELLS, depolarization by high K ϩ induces Ca 2ϩ release from intracellular stores mediated both by ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate (IP 3 ) receptors (IP 3 Rs) (11,18). The kinetics of the resulting Ca 2ϩ

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“…This construct has been previously characterized (Jiang et al, 2004). NFAT and MEF2 sensor constructs containing multimerized NFAT and MEF2 binding sites, respectively, coupled to the luciferase gene (3 µg/35 mm dish) were kindly provided by E. Olson (University of Texas Southwestern Medical Center, Dallas, TX).…”

Section: Dna Transfectionsmentioning

confidence: 99%

“…The fast MyHCIIa promoter was activated by increased calcium, NFAT and MEF2 (Allen and Leinwand, 2002). The avian slow MyHC2 promoter in slow muscle fibers is activated by both NFAT and MEF2, and both are required for innervationinduced expression of the slow muscle fiber phenotype (Jiang et al, 2004). Furthermore, regulation of NFAT transcriptional activity was fiber-type dependent.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of ryanodine receptor 1 in fast skeletal muscle fibers induces a fast-to-slow muscle fiber type transition

Jordan

Jiang

et al. 2004

Journal of Cell Science

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Skeletal muscle fiber type is regulated by innervation-induced cell signaling including calcium release mechanisms that lead to transcriptional activation of fiber type-specific genes. Avian fast pectoralis major (PM) and slow medial adductor (MA) muscles differentially control expression of the slow myosin heavy chain 2 (slow MyHC2) gene. We report here that slow MyHC2 gene expression in fast PM muscle fibers is repressed by endogenous activity of the ryanodine receptor 1 (RyR1). Inhibition of RyR1 with ryanodine led to expression of the slow MyHC2 gene in innervated PM muscle fibers in vitro. Administration of ryanodine to innervated PM muscle fibers also decreased protein kinase C (PKC) activity, the reduction of which is necessary for slow MyHC2 gene expression in both PM and MA muscle fibers. Furthermore, RyR1 inhibition increased slow MyHC2 promoter activity in innervated PM muscle fibers and enhanced transcriptional activities of nuclear factor of activated T cells (NFAT) and myocyte enhancer factor 2 (MEF2), as well as their interactions with their respective binding sites of the slow MyHC2 promoter. These results indicate that RyR1 activity in innervated fast PM muscle fibers contributes to the cell type-specific repression of slow muscle specific genes.

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Innervation‐dependent and fiber type‐specific transcriptional regulation of the slow myosin heavy chain 2 promoter in avian skeletal muscle fibers

Cited by 23 publications

References 62 publications

Sox6 is required for normal fiber type differentiation of fetal skeletal muscle in mice

Sox6 is required for normal fiber type differentiation of fetal skeletal muscle in mice

NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells

Inhibition of ryanodine receptor 1 in fast skeletal muscle fibers induces a fast-to-slow muscle fiber type transition

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