MRF4 can substitute for myogenin during early stages of myogenesis

Zhu, Zhimin; Miller, Jeffrey B.

doi:10.1002/(sici)1097-0177(199706)209:2<233::aid-aja9>3.0.co;2-j

Cited by 48 publications

(22 citation statements)

References 51 publications

(2 reference statements)

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“…In particular, we examined regeneration in mice carrying a transgene in which expression of MRF4 is under control of a myogenin promoter fragment. 14,15 We show that MRF4 is expressed sooner after injury in transgenic muscles than in wild-type muscles. In addition, premature expression of MRF4 from the transgene was accompanied by a similarly premature expression of the endogenous MRF4 gene, suggesting that MRF4 acts in a positive feedback loop to regulate its own expression in regenerating muscle.…”

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confidence: 72%

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Regeneration of Transgenic Skeletal Muscles with Altered Timing of Expression of the Basic Helix-Loop-Helix Muscle Regulatory Factor MRF4

Pavlath

Dominov

Kegley

et al. 2003

The American Journal of Pathology

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In regenerating muscle cells, muscle regulatory factor (MRF) 4 is normally the last of the four MRFs to be expressed. To analyze how the timing of MRF4 expression affects muscle regeneration, we compared regeneration after local freeze injury of muscles from wild-type mice with muscles from transgenic mice in which MRF4 expression was under control of an ϳ1.6-kb fragment of the myogenin promoter. Three days after injury, masseter and tibialis anterior (TA) muscles in wild-type mice expressed little or no MRF4 mRNA; whereas these muscles in transgenic mice expressed abundant MRF4 mRNA from both the transgene and the endogenous gene. Thus, MRF4 up-regulation was accelerated in transgenic compared to wild-type regenerating muscles, and expression of the transgene appeared to activate, perhaps indirectly, expression of the endogenous MRF4 gene. At 11 days after injury, regeneration, as measured by cross-sectional area and density of regenerated fibers, was significantly impaired in transgenic TA compared to wild-type TA, whereas at 19 days after injury both transgenic and TA muscle fibers had fully recovered to preinjury values. Regeneration of masseter muscles, which normally regenerate much less completely than TA muscles, was unaffected by the transgene. Thus, the timing of MRF4 up-regulation, as well as additional muscle-specific factors, can determine the progress of muscle regeneration. Regeneration of skeletal muscles after injury and formation of skeletal muscles during development are both regulated by a family of muscle-specific, basic helixloop-helix transcription factors, including muscle regulatory factor (MRF) 4, myogenin, MyoD, and Myf-5.

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confidence: 72%

“…14,15 Probes for myogenin, MyoD, and Myf-5 mRNAs were also used as previously described. 14,15,18 Consistent results were found when RNAs were obtained from multiple muscles (for replicates, from two to four muscles were analyzed; representative blots are shown).…”

Section: Transgenic Mice Genotyping Mrna Analysesmentioning

confidence: 99%

Regeneration of Transgenic Skeletal Muscles with Altered Timing of Expression of the Basic Helix-Loop-Helix Muscle Regulatory Factor MRF4

Pavlath

Dominov

Kegley

et al. 2003

The American Journal of Pathology

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“…It appears, therefore, that complex signaling events from surrounding embryonic tissues are integrated by complex regulatory elements at the Myf5 and Myod loci to accomplish a simple binary decision: whether or not to express Myod or (Zhu and Miller, 1997), demonstrating a partly redundant role of Mrf4 and Myog in terminal differentiation.…”

Section: Myod and Myf5: Nodal Points In Skeletal Muscle Specificationmentioning

confidence: 99%

The circuitry of a master switch: Myod and the regulation of skeletal muscle gene transcription

2005

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The cloning of Myod, a master switch for skeletal muscle In 1979, Taylor and Jones demonstrated that treating the mouse fibroblast cell line 10T1/2 with the demethylating agent 5-azacytidine generated clones with a skeletal muscle phenotypeThe expression of Myod is sufficient to convert a fibroblast to a skeletal muscle cell, and, as such, is a model system in developmental biology for studying how a single initiating event can orchestrate a highly complex and predictable response. Recent findings indicate that Myod functions in an instructive chromatin context and directly regulates genes that are expressed throughout the myogenic program, achieving promoter-specific regulation of its own binding and activity through a feed-forward mechanism. These studies are beginning to merge our understanding of how lineage-specific information is encoded in chromatin with how master regulatory factors drive programs of cell differentiation. Summary

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“…Indeed, Myer et al (1997), using chimeric mice containing both myogenin null and wildtype cells, showed that myogenin is required in vivo to establish an extracellular environment compatible with myoblast fusion. Yet, myogen-esis can be partly rescued in myogeninϪ/Ϫ embryos by a myogenin promoter-MRF4 transgene (Zhu and Miller, 1997). Furthermore, in myogenin-null embryonic stem (ES) cells, large fully differentiated muscle fibers are recovered by overexpression of MRF4 (Sumariwalla and Klein, 2001) but not of MyoD (Myer et al, 2001).…”

Section: Mrf Knock-out Micementioning

confidence: 99%

Myogenic regulatory factors: Redundant or specific functions? Lessons from Xenopus

Chanoine

Gaspera

Charbonnier

2004

Developmental Dynamics

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MRF4 can substitute for myogenin during early stages of myogenesis

Cited by 48 publications

References 51 publications

Regeneration of Transgenic Skeletal Muscles with Altered Timing of Expression of the Basic Helix-Loop-Helix Muscle Regulatory Factor MRF4

Regeneration of Transgenic Skeletal Muscles with Altered Timing of Expression of the Basic Helix-Loop-Helix Muscle Regulatory Factor MRF4

The circuitry of a master switch: Myod and the regulation of skeletal muscle gene transcription

Myogenic regulatory factors: Redundant or specific functions? Lessons from Xenopus

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