rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
2
|
pubmed:dateCreated |
1995-2-22
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pubmed:abstractText |
Myogenin, a member of the MyoD family of helix-loop-helix proteins, can induce myogenesis in a wide range of cell types. In addition to activating muscle structural genes, members of the MyoD family can autoactivate their own and cross-activate one another's expression in transfected cells. This has led to the hypothesis that autoregulatory loops among these factors provide a mechanism for amplifying and maintaining the muscle-specific gene expression program in vivo. Here, we make use of myogenin-null mice to directly test this hypothesis. To investigate whether the myogenin protein autoregulates the myogenin gene during embryogenesis, we introduced a myogenin-lacZ transgene into mice harboring a null mutation at the myogenin locus. Despite a severe deficiency of skeletal muscle in myogenin-null neonates, the myogenin-lacZ transgene was expressed normally in myogenic cells throughout embryogenesis. These results show that myogenin is not required for regulation of the myogenin gene and argue against the existence of a myogenin autoregulatory loop in the embryo.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1310995,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1315077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1321521,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1324403,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1328870,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1330322,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1334962,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1423602,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1649701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1652425,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1656214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1696180,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1715299,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-1995417,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2045411,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2300571,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2311584,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2473006,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2537150,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2546677,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2552320,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2560751,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2583111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2721498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2887293,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-2897631,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-3690668,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-7929574,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8026334,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8288123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8375340,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8384837,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8391506,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8392225,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8393145,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8393146,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7831329-8504933
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Jan
|
pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
17
|
pubmed:volume |
92
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
561-5
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7831329-Animals,
pubmed-meshheading:7831329-Animals, Newborn,
pubmed-meshheading:7831329-Embryo, Mammalian,
pubmed-meshheading:7831329-Female,
pubmed-meshheading:7831329-Gene Expression Regulation,
pubmed-meshheading:7831329-Genes, Reporter,
pubmed-meshheading:7831329-Male,
pubmed-meshheading:7831329-Mice,
pubmed-meshheading:7831329-Mice, Inbred C57BL,
pubmed-meshheading:7831329-Mice, Inbred CBA,
pubmed-meshheading:7831329-Mice, Transgenic,
pubmed-meshheading:7831329-Muscles,
pubmed-meshheading:7831329-Myogenin,
pubmed-meshheading:7831329-Promoter Regions, Genetic,
pubmed-meshheading:7831329-Recombinant Fusion Proteins,
pubmed-meshheading:7831329-Stem Cells,
pubmed-meshheading:7831329-Tongue,
pubmed-meshheading:7831329-beta-Galactosidase
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pubmed:year |
1995
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pubmed:articleTitle |
Activation of the myogenin promoter during mouse embryogenesis in the absence of positive autoregulation.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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