NDLI: Runx1 prevents wasting, myofibrillar disorganization, and autophagy of skeletal muscle

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Runx1 prevents wasting, myofibrillar disorganization, and autophagy of skeletal muscle

Content Provider	PubMed Central
Author	Wang, Xiaoxia Blagden, Chris Fan, Jihua Nowak, Scott J. Taniuchi, Ichiro Littman, Dan R. Burden, Steven J.
Copyright Year	2005
Abstract	Disruptions in the use of skeletal muscle lead to muscle atrophy. After short periods of disuse, muscle atrophy is reversible, and even after prolonged periods of inactivity, myofiber degeneration is uncommon. The pathways that regulate atrophy, initiated either by peripheral nerve damage, immobilization, aging, catabolic steroids, or cancer cachexia, however, are poorly understood. Previously, we found that Runx1 (AML1), a DNA-binding protein that is homologous to Drosophila Runt and has critical roles in hematopoiesis and leukemogenesis, is poorly expressed in innervated muscle, but strongly induced in muscle shortly after denervation. To determine the function of Runx1 in skeletal muscle, we generated mice in which Runx1 was selectively inactivated in muscle. Here, we show that Runx1 is required to sustain muscle by preventing denervated myofibers from undergoing myofibrillar disorganization and autophagy, structural defects found in a variety of congenital myopathies. We find that only 29 genes, encoding ion channels, signaling molecules, and muscle structural proteins, depend upon Runx1 expression, suggesting that their misregulation causes the dramatic muscle wasting. These findings demonstrate an unexpected role for electrical activity in regulating muscle wasting, and indicate that muscle disuse induces compensatory mechanisms that limit myofiber atrophy. Moreover, these results suggest that reduced muscle activity could cause or contribute to congenital myopathies if Runx1 or its target genes were compromised.
Related Links	http://dx.doi.org/10.1101/gad.1318305
Ending Page	1722
Page Count	8
Starting Page	1715
File Format	PDF
ISSN	08909369
Journal	Genes & Development
Issue Number	14
Volume Number	19
Language	English
Publisher	Cold Spring Harbor Laboratory Press
Publisher Date	2005-07-15
Access Restriction	Open
Rights Holder	Cold Spring Harbor Laboratory Press
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Genetics Developmental Biology

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