Mice Lacking Homer 1 Exhibit a Skeletal Myopathy Characterized by Abnormal Transient Receptor Potential Channel Activity

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Published inMolecular and Cellular Biology Vol. 28; no. 8; pp. 2637 - 2647
Main Authors Stiber, Jonathan A., Zhang, Zhu-Shan, Burch, Jarrett, Eu, Jerry P., Zhang, Sarah, Truskey, George A., Seth, Malini, Yamaguchi, Naohiro, Meissner, Gerhard, Shah, Ripal, Worley, Paul F., Williams, R. Sanders, Rosenberg, Paul B.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.04.2008
Taylor & Francis
American Society for Microbiology (ASM)
Subjects
Animals
Calcium Signaling
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cells, Cultured
Disease Models, Animal
Gene Deletion
Gene Expression Regulation
Homer Scaffolding Proteins
Mice
Mice, Knockout
Muscle Contraction
Muscular Dystrophies - genetics
Muscular Dystrophies - pathology
Muscular Dystrophies - physiopathology
Protein Binding
TRPC Cation Channels - genetics
TRPC Cation Channels - metabolism
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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList Transient receptor potential (TRP) channels are nonselective cation channels, several of which are expressed in striated muscle. Because the scaffolding protein Homer 1 has been implicated in TRP channel regulation, we hypothesized that Homer proteins play a significant role in skeletal muscle function. Mice lacking Homer 1 exhibited a myopathy characterized by decreased muscle fiber cross-sectional area and decreased skeletal muscle force generation. Homer 1 knockout myotubes displayed increased basal current density and spontaneous cation influx. This spontaneous cation influx in Homer 1 knockout myotubes was blocked by reexpression of Homer 1b, but not Homer 1a, and by gene silencing of TRPC1. Moreover, diminished Homer 1 expression in mouse models of Duchenne's muscular dystrophy suggests that loss of Homer 1 scaffolding of TRP channels may contribute to the increased stretch-activated channel activity observed in mdx myofibers. These findings provide direct evidence that Homer 1 functions as an important scaffold for TRP channels and regulates mechanotransduction in skeletal muscle.
Transient receptor potential (TRP) channels are nonselective cation channels, several of which are expressed in striated muscle. Because the scaffolding protein Homer 1 has been implicated in TRP channel regulation, we hypothesized that Homer proteins play a significant role in skeletal muscle function. Mice lacking Homer 1 exhibited a myopathy characterized by decreased muscle fiber cross-sectional area and decreased skeletal muscle force generation. Homer 1 knockout myotubes displayed increased basal current density and spontaneous cation influx. This spontaneous cation influx in Homer 1 knockout myotubes was blocked by reexpression of Homer 1b, but not Homer 1a, and by gene silencing of TRPC1. Moreover, diminished Homer 1 expression in mouse models of Duchenne's muscular dystrophy suggests that loss of Homer 1 scaffolding of TRP channels may contribute to the increased stretch-activated channel activity observed in mdx myofibers. These findings provide direct evidence that Homer 1 functions as an important scaffold for TRP channels and regulates mechanotransduction in skeletal muscle.
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
Author Jonathan A. Stiber
Malini Seth
Zhu-Shan Zhang
Paul B. Rosenberg
Jerry P. Eu
Paul F. Worley
Naohiro Yamaguchi
George A. Truskey
Ripal Shah
Jarrett Burch
R. Sanders Williams
Sarah Zhang
Gerhard Meissner
AuthorAffiliation Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, 1 Department of Biomedical Engineering, Duke University, Durham, North Carolina 27710, 2 Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, 3 Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland 21205 4
AuthorAffiliation_xml – name: Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, 1 Department of Biomedical Engineering, Duke University, Durham, North Carolina 27710, 2 Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, 3 Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland 21205 4
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Corresponding author. Mailing address: Department of Medicine, Duke University Medical Center, 4321 Medical Park Drive, Suite 200, Durham, NC 27704. Phone: (919) 479-2315. Fax: (919) 477-0632. E-mail: rosen029@mc.duke.edu
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Transient receptor potential (TRP) channels are nonselective cation channels, several of which are expressed in striated muscle. Because the scaffolding...
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StartPage 2637
SubjectTerms Animals
Calcium Signaling
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cells, Cultured
Disease Models, Animal
Gene Deletion
Gene Expression Regulation
Homer Scaffolding Proteins
Mice
Mice, Knockout
Muscle Contraction
Muscular Dystrophies - genetics
Muscular Dystrophies - pathology
Muscular Dystrophies - physiopathology
Protein Binding
TRPC Cation Channels - genetics
TRPC Cation Channels - metabolism
Title Mice Lacking Homer 1 Exhibit a Skeletal Myopathy Characterized by Abnormal Transient Receptor Potential Channel Activity
URI http://mcb.asm.org/content/28/8/2637.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.01601-07
https://www.ncbi.nlm.nih.gov/pubmed/18268005
https://search.proquest.com/docview/19890657
https://pubmed.ncbi.nlm.nih.gov/PMC2293116
Volume 28
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