Differential expression of C-protein isoforms in developing and degenerating mouse striated muscles

With the aim of clarifying the roles of C‐protein isoforms in developing mammalian skeletal muscle, we cloned the complementary DNA (cDNAs) encoding mouse fast (F) and slow (S) skeletal muscle C‐proteins and determined their entire sequences. Northern blotting with these cDNAs together with mouse ca...

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Veröffentlicht in:Muscle & nerve 1999-02, Vol.22 (2), p.196-207
Hauptverfasser: Kurasawa, Mariko, Sato, Naruki, Matsuda, Ayako, Koshida, Sumito, Totsuka, Tsuyoshi, Obinata, Takashi
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container_end_page 207
container_issue 2
container_start_page 196
container_title Muscle & nerve
container_volume 22
creator Kurasawa, Mariko
Sato, Naruki
Matsuda, Ayako
Koshida, Sumito
Totsuka, Tsuyoshi
Obinata, Takashi
description With the aim of clarifying the roles of C‐protein isoforms in developing mammalian skeletal muscle, we cloned the complementary DNA (cDNAs) encoding mouse fast (F) and slow (S) skeletal muscle C‐proteins and determined their entire sequences. Northern blotting with these cDNAs together with mouse cardiac (C) C‐protein cDNA was performed. It revealed that in adult mice, C, F, and S isoforms are expressed in a tissue‐specific fashion, although the messages for both F and S isoforms are transcribed in extensor digitorum longus muscle, which has been categorized as a fast muscle. In addition, although C isoform is expressed first and transiently during development of chicken skeletal muscles, C isoform is not expressed in mouse skeletal muscles at all through the developmental stages; S isoform is first expressed, followed by the appearance of F isoform. Finally, in dystrophic mouse skeletal muscles, the expression of S isoform is increased as it is in dystrophic chicken muscle. These observations suggest that mutations in C isoform (MyBP‐C) do not lead to any disturbance in skeletal muscle, although they may lead to familial hypertrophic cardiomyopathy. We also suggest that the expression of S isoform may be stimulated in degenerating human dystrophic muscles. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 196–207, 1999
doi_str_mv 10.1002/(SICI)1097-4598(199902)22:2<196::AID-MUS7>3.0.CO;2-E
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Neuromuscular diseases</topic><topic>DNA, Complementary - analysis</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Humans</topic><topic>Laminin - genetics</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred ICR</topic><topic>Mice, Knockout</topic><topic>Molecular Sequence Data</topic><topic>mouse muscle development</topic><topic>Muscle Development</topic><topic>Muscle Fibers, Fast-Twitch - metabolism</topic><topic>Muscle Fibers, Slow-Twitch - metabolism</topic><topic>Muscle Proteins - genetics</topic><topic>Muscle, Skeletal - growth &amp; development</topic><topic>Muscle, Skeletal - metabolism</topic><topic>muscular dystrophy</topic><topic>Muscular Dystrophy, Animal - genetics</topic><topic>Muscular Dystrophy, Animal - metabolism</topic><topic>Myocardium - metabolism</topic><topic>myosin-binding protein</topic><topic>Neurology</topic><topic>Protein Isoforms - genetics</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Sequence Analysis, DNA</topic><topic>Sequence Homology, Amino Acid</topic><topic>Space life sciences</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kurasawa, Mariko</creatorcontrib><creatorcontrib>Sato, Naruki</creatorcontrib><creatorcontrib>Matsuda, Ayako</creatorcontrib><creatorcontrib>Koshida, Sumito</creatorcontrib><creatorcontrib>Totsuka, Tsuyoshi</creatorcontrib><creatorcontrib>Obinata, Takashi</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Muscle &amp; nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kurasawa, Mariko</au><au>Sato, Naruki</au><au>Matsuda, Ayako</au><au>Koshida, Sumito</au><au>Totsuka, Tsuyoshi</au><au>Obinata, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential expression of C-protein isoforms in developing and degenerating mouse striated muscles</atitle><jtitle>Muscle &amp; nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>1999-02</date><risdate>1999</risdate><volume>22</volume><issue>2</issue><spage>196</spage><epage>207</epage><pages>196-207</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>With the aim of clarifying the roles of C‐protein isoforms in developing mammalian skeletal muscle, we cloned the complementary DNA (cDNAs) encoding mouse fast (F) and slow (S) skeletal muscle C‐proteins and determined their entire sequences. Northern blotting with these cDNAs together with mouse cardiac (C) C‐protein cDNA was performed. It revealed that in adult mice, C, F, and S isoforms are expressed in a tissue‐specific fashion, although the messages for both F and S isoforms are transcribed in extensor digitorum longus muscle, which has been categorized as a fast muscle. In addition, although C isoform is expressed first and transiently during development of chicken skeletal muscles, C isoform is not expressed in mouse skeletal muscles at all through the developmental stages; S isoform is first expressed, followed by the appearance of F isoform. Finally, in dystrophic mouse skeletal muscles, the expression of S isoform is increased as it is in dystrophic chicken muscle. These observations suggest that mutations in C isoform (MyBP‐C) do not lead to any disturbance in skeletal muscle, although they may lead to familial hypertrophic cardiomyopathy. We also suggest that the expression of S isoform may be stimulated in degenerating human dystrophic muscles. © 1999 John Wiley &amp; Sons, Inc. Muscle Nerve 22: 196–207, 1999</abstract><cop>New York</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>10024132</pmid><doi>10.1002/(SICI)1097-4598(199902)22:2&lt;196::AID-MUS7&gt;3.0.CO;2-E</doi><tpages>12</tpages></addata></record>
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subjects Amino Acid Sequence
Animals
Base Sequence
Biological and medical sciences
Blotting, Northern
C-protein
Carrier Proteins
cDNA cloning
Cloning, Molecular
Diseases of striated muscles. Neuromuscular diseases
DNA, Complementary - analysis
Gene Expression Regulation, Developmental
Humans
Laminin - genetics
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Inbred ICR
Mice, Knockout
Molecular Sequence Data
mouse muscle development
Muscle Development
Muscle Fibers, Fast-Twitch - metabolism
Muscle Fibers, Slow-Twitch - metabolism
Muscle Proteins - genetics
Muscle, Skeletal - growth & development
Muscle, Skeletal - metabolism
muscular dystrophy
Muscular Dystrophy, Animal - genetics
Muscular Dystrophy, Animal - metabolism
Myocardium - metabolism
myosin-binding protein
Neurology
Protein Isoforms - genetics
RNA, Messenger - biosynthesis
Sequence Analysis, DNA
Sequence Homology, Amino Acid
Space life sciences
title Differential expression of C-protein isoforms in developing and degenerating mouse striated muscles
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