Switching of actin isoforms in skeletal muscle differentiation using mouse ES cells

Mizuno, Yota; Suzuki, Mayu; Nakagawa, Hiroki; Ninagawa, Nana; Torihashi, Shigeko

doi:10.1007/s00418-009-0650-9

Cited by 9 publications

(8 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A crucial step during early postnatal skeletal muscle development is the replacement of smooth muscle (α-SMA) and cardiac muscle (α-CAA) α-actin by skeletal muscle (α-SKA) α-actin (18, 19). This exchange requires the coordinated release of actin subunits, and cofilin2, a putative CAP2 interaction partner (9), has been implicated therein (20).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function

Kepser

Damar

Cicco

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Actin filaments (F-actin) are key components of sarcomeres, the basic contractile units of skeletal muscle myofibrils. A crucial step during myofibril differentiation is the sequential exchange of α-actin isoforms from smooth muscle (α-SMA) and cardiac (α-CAA) to skeletal muscle α-actin (α-SKA) that, in mice, occurs during early postnatal life. This “α-actin switch” requires the coordinated activity of actin regulators because it is vital that sarcomere structure and function are maintained during differentiation. The molecular machinery that controls the α-actin switch, however, remains enigmatic. Cyclase-associated proteins (CAP) are a family of actin regulators with largely unknown physiological functions. We here report a function for CAP2 in regulating the α-actin exchange during myofibril differentiation. This α-actin switch was delayed in systemic CAP2 mutant mice, and myofibrils remained in an undifferentiated stage at the onset of the often excessive voluntary movements in postnatal mice. The delay in the α-actin switch coincided with the onset of motor function deficits and histopathological changes including a high frequency of type IIB ring fibers. Our data suggest that subtle disturbances of postnatal F-actin remodeling are sufficient for predisposing muscle fibers to form ring fibers. Cofilin2, a putative CAP2 interaction partner, has been recently implicated in myofibril actin cytoskeleton differentiation, and the myopathies in cofilin2 and CAP2 mutant mice showed striking similarities. We therefore propose a model in which CAP2 and cofilin2 cooperate in actin regulation during myofibril differentiation.

show abstract

Section: Resultsmentioning

confidence: 99%

“…S9 A , refs. 18 and 19). Specifically, α-SKA replaces α-SMA and α-CAA to become the major α-actin in differentiated myofibrils.…”

Section: Discussionmentioning

confidence: 98%

CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function

Kepser

Damar

Cicco

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Electron microscopy analysis of mouse and human PSC-derived myofibers revealed that they exhibit highly organized sarcomeric units, reminiscent of the cytoarchitecture found in vivo (Hirsch et al, 1998;Skoglund et al, 2014). Myofibrils generated in these fibers can exhibit the appropriate organization of MyHC, troponin T, nebulin and titin, and undergo the stage-specific developmental transitions through α-actins (cardiac to skeletal) and MyHC (embryonic, fetal, and perinatal/fast) isoforms (Chal et al, 2015;Hirsch et al, 1998;Mizuno et al, 2009;Rohwedel et al, 1998b). Furthermore, desmin null mESCs have been used to demonstrate the important role of desmin in the early formation of myotubes (Höllrigl et al, 2002;Weitzer et al, 1995).…”

Section: Myofiber Maturation In Vitro Sarcomeres and Structural Assemblymentioning

confidence: 99%

Making muscle: skeletal myogenesisin vivoandin vitro

2017

View full text Add to dashboard Cite

Skeletal muscle is the largest tissue in the body and loss of its function or its regenerative properties results in debilitating musculoskeletal disorders. Understanding the mechanisms that drive skeletal muscle formation will not only help to unravel the molecular basis of skeletal muscle diseases, but also provide a roadmap for recapitulating skeletal myogenesis in vitro from pluripotent stem cells (PSCs). PSCs have become an important tool for probing developmental questions, while differentiated cell types allow the development of novel therapeutic strategies. In this Review, we provide a comprehensive overview of skeletal myogenesis from the earliest premyogenic progenitor stage to terminally differentiated myofibers, and discuss how this knowledge has been applied to differentiate PSCs into muscle fibers and their progenitors in vitro.

show abstract

“…By using cultivated mouse embryonic stem cells, this switching of actin isoforms was demonstrated by Mizuno et al (2009) for the Wrst time in vitro. Only after myotube formation, the cardiac type actin decreased and -skeletal actin increased and remained as the main actin component in mature skeletal muscle.…”

Section: Skeletal Musclementioning

confidence: 97%

Extending the knowledge in histochemistry and cell biology

Heupel

Drenckhahn

2009

Histochem Cell Biol

View full text Add to dashboard Cite

Central to modern Histochemistry and Cell Biology stands the need for visualization of cellular and molecular processes. In the past several years, a variety of techniques has been achieved bridging traditional light microscopy, fluorescence microscopy and electron microscopy with powerful software-based post-processing and computer modeling. Researchers now have various tools available to investigate problems of interest from bird's- up to worm's-eye of view, focusing on tissues, cells, proteins or finally single molecules. Applications of new approaches in combination with well-established traditional techniques of mRNA, DNA or protein analysis have led to enlightening and prudent studies which have paved the way toward a better understanding of not only physiological but also pathological processes in the field of cell biology. This review is intended to summarize articles standing for the progress made in "histo-biochemical" techniques and their manifold applications.

show abstract

Switching of actin isoforms in skeletal muscle differentiation using mouse ES cells

Cited by 9 publications

References 11 publications

CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function

CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function

Making muscle: skeletal myogenesisin vivoandin vitro

Extending the knowledge in histochemistry and cell biology

Contact Info

Product

Resources

About