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

Producción científica: Article › revisión exhaustiva

58 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	493-502
Número de páginas	10
Publicación	Cell
Volumen	62
N.º	3
DOI	https://doi.org/10.1016/0092-8674(90)90014-6
Estado	Published - ago 10 1990

Nota bibliográfica

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.

Financiación

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.

Financiadores	Número del financiador
Katharine McCormick Fund for Women in Science
National Science Foundation Arctic Social Science Program	DCB 8417089
National Institutes of Health (NIH)	HD20203
American the American Heart Association
Muscular Dystrophy Association
Israel National Road Safety Authority
Eunice Kennedy Shriver National Institute of Child Health and Human Development	R01HD018179

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

Acceder al documento

10.1016/0092-8674(90)90014-6

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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

AU - Hall, Zach W.

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

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

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