Differential expression of two distinct MyoD genes in Xenopus.

J. B. Scales, E. N. Olson, M. Perry

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

We previously reported the isolation of several complementary DNAs from Xenopus laevis that encode distinct MyoD proteins. Two of these genes, Xlmf1 and Xlmf25, appear to represent a gene duplication as a consequence of the polyploid Xenopus genome. Although both MyoD genes are expressed exclusively in skeletal muscle in adult animals, they have very different temporal patterns of expression in early development. In the present work, we show that Xlmf1 transcripts rapidly accumulated to high levels shortly after activation of the zygotic genome at the midblastula transition. In contrast, Xlmf25 was expressed as a maternal transcript that was maintained at a relatively constant level throughout early development. Xlmf25, like Xlmf1, was capable of converting 10T1/2 fibroblasts to a myogenic phenotype. In addition, both proteins directly transactivated reporter genes linked to muscle-specific regulatory elements. Xlmf1 was twice as active in this regard as Xlmf25 and required a carboxy-terminal domain for its function. The absence of apparent effect of the maternally expressed myogenic gene in early embryos, but not in transfected fibroblasts, suggests the existence of regulatory mechanisms that repress the function of this gene in cells with nonmuscle fates during early amphibian development.

Original languageEnglish (US)
Pages (from-to)619-629
Number of pages11
JournalCell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
Volume2
Issue number12
StatePublished - Dec 1991

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Xenopus
Genes
MyoD Protein
Fibroblasts
Genome
Polyploidy
Gene Duplication
Xenopus laevis
Amphibians
Reporter Genes
Skeletal Muscle
Embryonic Structures
Complementary DNA
Mothers
Phenotype
Muscles
Proteins

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

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abstract = "We previously reported the isolation of several complementary DNAs from Xenopus laevis that encode distinct MyoD proteins. Two of these genes, Xlmf1 and Xlmf25, appear to represent a gene duplication as a consequence of the polyploid Xenopus genome. Although both MyoD genes are expressed exclusively in skeletal muscle in adult animals, they have very different temporal patterns of expression in early development. In the present work, we show that Xlmf1 transcripts rapidly accumulated to high levels shortly after activation of the zygotic genome at the midblastula transition. In contrast, Xlmf25 was expressed as a maternal transcript that was maintained at a relatively constant level throughout early development. Xlmf25, like Xlmf1, was capable of converting 10T1/2 fibroblasts to a myogenic phenotype. In addition, both proteins directly transactivated reporter genes linked to muscle-specific regulatory elements. Xlmf1 was twice as active in this regard as Xlmf25 and required a carboxy-terminal domain for its function. The absence of apparent effect of the maternally expressed myogenic gene in early embryos, but not in transfected fibroblasts, suggests the existence of regulatory mechanisms that repress the function of this gene in cells with nonmuscle fates during early amphibian development.",
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N2 - We previously reported the isolation of several complementary DNAs from Xenopus laevis that encode distinct MyoD proteins. Two of these genes, Xlmf1 and Xlmf25, appear to represent a gene duplication as a consequence of the polyploid Xenopus genome. Although both MyoD genes are expressed exclusively in skeletal muscle in adult animals, they have very different temporal patterns of expression in early development. In the present work, we show that Xlmf1 transcripts rapidly accumulated to high levels shortly after activation of the zygotic genome at the midblastula transition. In contrast, Xlmf25 was expressed as a maternal transcript that was maintained at a relatively constant level throughout early development. Xlmf25, like Xlmf1, was capable of converting 10T1/2 fibroblasts to a myogenic phenotype. In addition, both proteins directly transactivated reporter genes linked to muscle-specific regulatory elements. Xlmf1 was twice as active in this regard as Xlmf25 and required a carboxy-terminal domain for its function. The absence of apparent effect of the maternally expressed myogenic gene in early embryos, but not in transfected fibroblasts, suggests the existence of regulatory mechanisms that repress the function of this gene in cells with nonmuscle fates during early amphibian development.

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