Interaction of the myogenic determination factor myogenin with E12 and a DNA target: mechanism and kinetics

Spinner, Daryl S.; Liu, Shaohua; Wang, Shaowen; Schmidt, John T.

doi:10.1006/jmbi.2002.5440

Cited by 22 publications

(17 citation statements)

References 66 publications

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“…No band was revealed if no antibody was added to the reaction mixture. Moreover, immunoprecipitation with the anti-CREB1 antibody did not precipitate DNA fragments of the 5Ј-flanking region of the AChR ␣ subunit gene, which does not contain the CRE cis element (47), or the AChR ε subunit coding region (Fig. 1B).…”

Section: Resultsmentioning

confidence: 99%

Inhibition of MuSK Expression by CREB Interacting with a CRE-Like Element and MyoD

Kim

Xiong

Mei

2005

Molecular and Cellular Biology

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The type I receptor-like protein tyrosine kinase MuSK is essential for the neuromuscular junction formation. MuSK expression is tightly regulated during development, but the underlying mechanisms were unclear. Here we identified a novel mechanism by which MuSK expression may be regulated. A cyclic AMP response element (CRE)-like element in the 5′-flanking region of the MuSK gene binds to CREB1 (CRE-binding protein 1). Mutation of this element increases the MuSK promoter activity, suggesting a role for CREB1 in attenuation of MuSK expression. Interestingly, CREB mutants unable to bind to DNA also inhibit MuSK promoter activity, suggesting a CRE-independent inhibitory mechanism. In agreement, CREB1 could inhibit a mutant MuSK transgene reporter whose CRE site was mutated. We provide evidence that CREB interacts directly with MyoD, a myogenic factor essential for MuSK expression in muscle cells. Suppression of CREB expression by small interfering RNA increases MuSK promoter activity. These results demonstrate an important role for CREB1 in the regulation of MuSK expression

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Section: Resultsmentioning

confidence: 99%

Inhibition of MuSK Expression by CREB Interacting with a CRE-Like Element and MyoD

Kim

Xiong

Mei

2005

Molecular and Cellular Biology

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“…Understanding how a single transcription factor such as MyoD can initiate distinct subprograms during development has profound impact on the understanding of gene regulatory network. Multiple mechanisms have been implicated to differentially modulate MyoD binding between growth and differentiation of muscle cells including heterodimerization with E-proteins such as E47/E12 (Spinner et al, 2002), interaction with Twist protein (Hamamori et al, 1997; Hebrok et al, 1997), interaction with the inhibitory Ids proteins (Chen et al, 1997), and posttranscriptional modifications of MyoD (Gillespie et al, 2009; Song et al, 1998) and its heterodimerization partners (Butler et al, 2009; Lluis et al, 2005; Mitsui et al, 1993). Importantly, none of these mechanisms adequately explain the discrete behavior in MyoD binding pattern on unique targets during two different stages of muscle development.…”

Section: Discussionmentioning

confidence: 99%

Snail Regulates MyoD Binding-Site Occupancy to Direct Enhancer Switching and Differentiation-Specific Transcription in Myogenesis

et al. 2012

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SUMMARY In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-Seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex binds and excludes MyoD from its targets. Notably, Snail binds E box motifs that are G/C rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevent MyoD occupancy on differentiation-specific regulatory elements, and the change from Snail to MyoD binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving myogenic regulatory factors (MRFs), Snai1/2, miR-30a, and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells.

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“…The basic region forms an extension of one of the α-helices of the HLH region and facilitates DNA binding. bHLH dimers specifically bind Ebox elements (CANNTG) found in the promoters and enhancers of most, if not all, muscle-specific genes (Apone and Hauschka, 1995;Spinner et al, 2002) although it is likely that nucleotide variation in the flanking regions and within the motif imparts some specificity (Ludolph and Konieczny, 1995). During myogenesis, the transcription factors Myf-5 and MyoD are required for the initial determination of the myogenic lineage.…”

Section: Introductionmentioning

confidence: 99%

Temperature and the expression of myogenic regulatory factors (MRFs) and myosin heavy chain isoforms during embryogenesis in the common carpCyprinus carpioL.

Cole

Hall

Martin

et al. 2004

Journal of Experimental Biology

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Interaction of the myogenic determination factor myogenin with E12 and a DNA target: mechanism and kinetics

Cited by 22 publications

References 66 publications

Inhibition of MuSK Expression by CREB Interacting with a CRE-Like Element and MyoD

Inhibition of MuSK Expression by CREB Interacting with a CRE-Like Element and MyoD

Snail Regulates MyoD Binding-Site Occupancy to Direct Enhancer Switching and Differentiation-Specific Transcription in Myogenesis

Temperature and the expression of myogenic regulatory factors (MRFs) and myosin heavy chain isoforms during embryogenesis in the common carpCyprinus carpioL.

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