Negative control of the helix-loop-helix family of myogenic regulators in the NFB mutant

Charlotte A. Peterson; Herman Gordon; Zach W. Hall; Bruce M. Paterson; Helen M. Blau

doi:10.1016/0092-8674(90)90014-6

Negative control of the helix-loop-helix family of myogenic regulators in the NFB mutant

Charlotte A. Peterson, Herman Gordon, Zach W. Hall, Bruce M. Paterson, Helen M. Blau

Physical Therapy

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58 Scopus citations

Abstract

We have characterized a nondifferentiating mouse muscle cell line, NFB, that represses the activity of the helix-loop-helix (HLH) family of myogenic regulators, yet expresses sarcomeric actins. The NFB MyoD gene is silent, but can be activated upon transfection of a long terminal region-controlled chicken MyoD cDNA, resulting in myogenesis. When NFB cells are fused with H9c2 rat muscle cells in heterokaryons, the level of rat MyoD transcripts declines. Thus, the stoichiometry of MyoD and the putative repressor controls myogenesis. Although NFB cells express myogenin and Myf-5 transcripts, the activity of these regulators is also repressed: myogenesis is not induced in 10T1 2 fibroblasts and is repressed in L6 muscle cells upon fusion with NFB cells. We conclude that the myogenic HLH regulators are not required for sarcomeric actin gene activation and that myogenesis is subject to dominant-negative control.

Original language	English
Pages (from-to)	493-502
Number of pages	10
Journal	Cell
Volume	62
Issue number	3
DOIs	https://doi.org/10.1016/0092-8674(90)90014-6
State	Published - Aug 10 1990

Bibliographical note

Funding Information:
Lassar for providing 101112 cells and the MyoD antibody and Dr. John Coleman for providing LGJl-C cells. We are indebted to Dr. Farzan Rastinejad for the test of anchorage independence of NFB cells, Marilyn Travis for assistance with graphics, and Dr. Matthew Sachs for advice on Northern blot analysis. We thank Drs. Gerald Crabtree, Juan Botas, and colleagues in the laboratory for helpful comments on the manuscript. This work was supported by the California Affiliate of the American Heart Association and the Katharine McCormick Fund for Women in Science (C. A. P.), an NRSA from the National Institutes of Health (H. G.), and grants from the National Institutes of Health (HD18179 and HD20203), the National Science Foundation (DCB 8417089), and the Muscular Dystrophy Association to H. M. B.

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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10.1016/0092-8674(90)90014-6

Cite this

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title = "Negative control of the helix-loop-helix family of myogenic regulators in the NFB mutant",

abstract = "We have characterized a nondifferentiating mouse muscle cell line, NFB, that represses the activity of the helix-loop-helix (HLH) family of myogenic regulators, yet expresses sarcomeric actins. The NFB MyoD gene is silent, but can be activated upon transfection of a long terminal region-controlled chicken MyoD cDNA, resulting in myogenesis. When NFB cells are fused with H9c2 rat muscle cells in heterokaryons, the level of rat MyoD transcripts declines. Thus, the stoichiometry of MyoD and the putative repressor controls myogenesis. Although NFB cells express myogenin and Myf-5 transcripts, the activity of these regulators is also repressed: myogenesis is not induced in 10T1 2 fibroblasts and is repressed in L6 muscle cells upon fusion with NFB cells. We conclude that the myogenic HLH regulators are not required for sarcomeric actin gene activation and that myogenesis is subject to dominant-negative control.",

author = "Peterson, {Charlotte A.} and Herman Gordon and Hall, {Zach W.} and Paterson, {Bruce M.} and Blau, {Helen M.}",

note = "Funding Information: Lassar for providing 101112 cells and the MyoD antibody and Dr. John Coleman for providing LGJl-C cells. We are indebted to Dr. Farzan Rastinejad for the test of anchorage independence of NFB cells, Marilyn Travis for assistance with graphics, and Dr. Matthew Sachs for advice on Northern blot analysis. We thank Drs. Gerald Crabtree, Juan Botas, and colleagues in the laboratory for helpful comments on the manuscript. This work was supported by the California Affiliate of the American Heart Association and the Katharine McCormick Fund for Women in Science (C. A. P.), an NRSA from the National Institutes of Health (H. G.), and grants from the National Institutes of Health (HD18179 and HD20203), the National Science Foundation (DCB 8417089), and the Muscular Dystrophy Association to H. M. B.",

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AU - Gordon, Herman

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AU - Paterson, Bruce M.

AU - Blau, Helen M.

N1 - Funding Information: Lassar for providing 101112 cells and the MyoD antibody and Dr. John Coleman for providing LGJl-C cells. We are indebted to Dr. Farzan Rastinejad for the test of anchorage independence of NFB cells, Marilyn Travis for assistance with graphics, and Dr. Matthew Sachs for advice on Northern blot analysis. We thank Drs. Gerald Crabtree, Juan Botas, and colleagues in the laboratory for helpful comments on the manuscript. This work was supported by the California Affiliate of the American Heart Association and the Katharine McCormick Fund for Women in Science (C. A. P.), an NRSA from the National Institutes of Health (H. G.), and grants from the National Institutes of Health (HD18179 and HD20203), the National Science Foundation (DCB 8417089), and the Muscular Dystrophy Association to H. M. B.

PY - 1990/8/10

Y1 - 1990/8/10

N2 - We have characterized a nondifferentiating mouse muscle cell line, NFB, that represses the activity of the helix-loop-helix (HLH) family of myogenic regulators, yet expresses sarcomeric actins. The NFB MyoD gene is silent, but can be activated upon transfection of a long terminal region-controlled chicken MyoD cDNA, resulting in myogenesis. When NFB cells are fused with H9c2 rat muscle cells in heterokaryons, the level of rat MyoD transcripts declines. Thus, the stoichiometry of MyoD and the putative repressor controls myogenesis. Although NFB cells express myogenin and Myf-5 transcripts, the activity of these regulators is also repressed: myogenesis is not induced in 10T1 2 fibroblasts and is repressed in L6 muscle cells upon fusion with NFB cells. We conclude that the myogenic HLH regulators are not required for sarcomeric actin gene activation and that myogenesis is subject to dominant-negative control.

AB - We have characterized a nondifferentiating mouse muscle cell line, NFB, that represses the activity of the helix-loop-helix (HLH) family of myogenic regulators, yet expresses sarcomeric actins. The NFB MyoD gene is silent, but can be activated upon transfection of a long terminal region-controlled chicken MyoD cDNA, resulting in myogenesis. When NFB cells are fused with H9c2 rat muscle cells in heterokaryons, the level of rat MyoD transcripts declines. Thus, the stoichiometry of MyoD and the putative repressor controls myogenesis. Although NFB cells express myogenin and Myf-5 transcripts, the activity of these regulators is also repressed: myogenesis is not induced in 10T1 2 fibroblasts and is repressed in L6 muscle cells upon fusion with NFB cells. We conclude that the myogenic HLH regulators are not required for sarcomeric actin gene activation and that myogenesis is subject to dominant-negative control.

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Negative control of the helix-loop-helix family of myogenic regulators in the NFB mutant

Abstract

Bibliographical note

ASJC Scopus subject areas

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