ArticleNucleic acids research1997
A muscle-specific enhancer within intron 1 of the human dystrophin gene is functionally dependent on single MEF-1/E box and MEF-2/AT-rich sequence motifs.
Article in Nucleic acids research, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 27 citations in OpenAlex.
- G9a inhibits MEF2C activity to control sarcomere assembly.Scientific reports · 2016Article
- The Mef2A transcription factor coordinately regulates a costamere gene program in cardiac muscle.The Journal of biological chemistry · 2011Article
- Contributions of selective knockout studies to understanding cholinesterase disposition and function.Chemico-biological interactions · 2010Article
- The deacetylase HDAC4 controls myocyte enhancing factor-2-dependent structural gene expression in response to neural activity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Myocyte-specific M-CAT and MEF-1 elements regulate G-protein gamma 3 gene (gamma3) expression in cardiac myocytes.DNA and cell biology · 2008Article
- Acetylcholinesterase expression in muscle is specifically controlled by a promoter-selective enhancesome in the first intron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In previous studies we have described a 5.0 kb Hin dIII fragment downstream of muscle exon 1 that exhibits properties consistent with a muscle-specific transcriptional enhancer. The goal of this study has been to identify the sequence elements responsible for muscle-specific enhancer activity. Functional studies indicated that this enhancer is active in pre- and post-differentiated H9C2(2-1) myoblasts but functions poorly in L6 and C2C12 myotubes. The core enhancer region was delimited to a 195 bp Spe I- Acc I fragment and sequence analysis identified three MEF-1/E box and two MEF-2/AT-rich motifs as potential muscle-specific regulatory domains. EMSA competition and DNase footprinting indicated that sequences within a 30 bp region containing single adjoining MEF-1/E box and MEF-2/AT-rich motifs are target binding sites for trans -acting factors expressed in H9C2(2-1) myotubes but not in L6 or C2C12 myotubes. Site-specific mutations within these motifs resulted in a significant reduction in enhancer activity in H9C2(2-1) myotubes. These results suggest that the mechanisms governing DMD gene expression in muscle are similar to those identified in other muscle-specific genes. However, the myogenic profile of enhancer activity and trans -acting factor binding suggests a more specialized role for this enhancer that is consistent with its potential involvement in dystrophin gene regulation in cardiac muscle.
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