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dc.contributor.authorUstanina, S
dc.contributor.authorCarvajal, J
dc.contributor.authorRigby, P
dc.contributor.authorBraun, T
dc.date.accessioned2018-08-31T14:54:26Z
dc.date.issued2009-01-02
dc.identifierhttps://doi.org/10.1634/stemcells.2006-0736
dc.identifier.citationSTEM CELLS, 2009, 25 (8), pp. 2006 - 2016
dc.identifier.issn1066-5099
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2489
dc.identifier.doi10.1634/stemcells.2006-0736
dc.description.abstractAbstract The myogenic factor Myf5 defines the onset of myogenesis in mammals during development. Mice lacking both Myf5 and MyoD fail to form myoblasts and are characterized by a complete absence of skeletal muscle at birth. To investigate the function of Myf5 in adult skeletal muscle, we generated Myf5 and mdx compound mutants, which are characterized by constant regeneration. Double mutant mice show an increase of dystrophic changes in the musculature, although these mice were viable and the degree of myopathy was modest. Myf5 mutant muscles show a small decrease in the number of muscle satellite cells, which was within the range of physiological variations. We also observed a significant delay in the regeneration of Myf5 deficient skeletal muscles after injury. Interestingly, Myf5 deficient skeletal muscles were able to even out this flaw during the course of regeneration, generating intact muscles 4 weeks after injury. Although we did not detect a striking reduction of MyoD positive activated myoblasts or of Myf5-LacZ positive cells in regenerating muscles, a clear decrease in the proliferation rate of satellite cell-derived myoblasts was apparent in satellite cell-derived cultures. The reduction of the proliferation rate of Myf5 mutant myoblasts was also reflected by a delayed transition from proliferation to differentiation, resulting in a reduced number of myotube nuclei after 6 and 7 days of culture. We reason that Myf5 supports efficient skeletal muscle regeneration by enabling transient myoblast amplification. Disclosure of potential conflicts of interest is found at the end of this article.
dc.format.extent2006 - 2016
dc.languageeng
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.subjectMuscle regeneration
dc.subjectMyf5
dc.subjectSatellite cells
dc.subjectStem cells
dc.subjectMuscle differentiation
dc.titleThe Myogenic Factor Myf5 Supports Efficient Skeletal Muscle Regeneration by Enabling Transient Myoblast Amplification
dc.typeJournal Article
rioxxterms.versionofrecord10.1634/stemcells.2006-0736
rioxxterms.licenseref.startdate2009-01-02
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfSTEM CELLS
pubs.issue8
pubs.notesdoi: 10.1634/stemcells.2006-0736
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Molecular Embryology
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Molecular Embryology
pubs.volume25
pubs.embargo.termsNot known
icr.researchteamMolecular Embryologyen_US
dc.contributor.icrauthorRigby, Peter William Jacken


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