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  1. Article ; Online: Distinct Activities of Myf5 and MyoD Indicate Separate Roles in Skeletal Muscle Lineage Specification and Differentiation.

    Conerly, Melissa L / Yao, Zizhen / Zhong, Jun Wen / Groudine, Mark / Tapscott, Stephen J

    Developmental cell

    2016  Volume 36, Issue 4, Page(s) 375–385

    Abstract: Most transcription factor families contain highly related paralogs generated by gene duplication, and functional divergence is generally accomplished by activation of distinct sets of genes by each member. Here we compare the molecular functions of Myf5 ... ...

    Abstract Most transcription factor families contain highly related paralogs generated by gene duplication, and functional divergence is generally accomplished by activation of distinct sets of genes by each member. Here we compare the molecular functions of Myf5 and MyoD, two highly related bHLH transcription factors that regulate skeletal muscle specification and differentiation. We find that MyoD and Myf5 bind the same sites genome-wide but have distinct functions: Myf5 induces histone acetylation without Pol II recruitment or robust gene activation, whereas MyoD induces histone acetylation, recruits Pol II, and robustly activates gene transcription. Therefore, the initial specification of the muscle lineage by Myf5 occurs without significant induction of gene transcription. Transcription of the skeletal muscle program is then achieved by the subsequent expression of MyoD, which binds to the same sites as Myf5, indicating that each factor regulates distinct steps in gene initiation and transcription at a shared set of binding sites.
    MeSH term(s) Animals ; Cell Differentiation/physiology ; Cell Lineage ; Gene Expression Regulation, Developmental/physiology ; Mice ; Muscle Proteins/metabolism ; Muscle, Skeletal/cytology ; Muscle, Skeletal/metabolism ; MyoD Protein/metabolism ; Myogenic Regulatory Factor 5/metabolism ; Transcriptional Activation/physiology
    Chemical Substances Muscle Proteins ; Myf5 protein, mouse ; MyoD Protein ; Myogenic Regulatory Factor 5
    Language English
    Publishing date 2016-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2016.01.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5742: Show issues Location:
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  2. Article ; Online: Polycomb-mediated repression during terminal differentiation: what don't you want to be when you grow up?

    Conerly, Melissa L / MacQuarrie, Kyle L / Fong, Abraham P / Yao, Zizhen / Tapscott, Stephen J

    Genes & development

    2011  Volume 25, Issue 10, Page(s) 997–1003

    Abstract: Chromatin-modifying enzymes are known to be critical components for the correct differentiation of embryonic stem cells into specific lineages, such as neurons. Recently, the role of Polycomb group proteins has been studied in the specification and ... ...

    Abstract Chromatin-modifying enzymes are known to be critical components for the correct differentiation of embryonic stem cells into specific lineages, such as neurons. Recently, the role of Polycomb group proteins has been studied in the specification and differentiation of muscle stem cells. In this perspective, we review a recent study by Juan and colleagues (pp. 789-794) in Genes & Development of the role of the polycomb group protein Ezh2 in muscle stem cells, and discuss the implications for general lineage restriction.
    MeSH term(s) Animals ; Cell Differentiation ; Drosophila ; Gene Expression Regulation, Developmental ; Humans ; Mice ; Muscle Development ; Muscle, Skeletal/cytology ; Muscle, Skeletal/metabolism ; Polycomb-Group Proteins ; Repressor Proteins/metabolism ; Stem Cells/cytology ; Stem Cells/metabolism ; Transcription Factors/metabolism
    Chemical Substances Polycomb-Group Proteins ; Repressor Proteins ; Transcription Factors
    Language English
    Publishing date 2011-05-16
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.2054311
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: DUX4-induced dsRNA and MYC mRNA stabilization activate apoptotic pathways in human cell models of facioscapulohumeral dystrophy.

    Shadle, Sean C / Zhong, Jun Wen / Campbell, Amy E / Conerly, Melissa L / Jagannathan, Sujatha / Wong, Chao-Jen / Morello, Timothy D / van der Maarel, Silvère M / Tapscott, Stephen J

    PLoS genetics

    2017  Volume 13, Issue 3, Page(s) e1006658

    Abstract: Facioscapulohumeral dystrophy (FSHD) is caused by the mis-expression of DUX4 in skeletal muscle cells. DUX4 is a transcription factor that activates genes normally associated with stem cell biology and its mis-expression in FSHD cells results in ... ...

    Abstract Facioscapulohumeral dystrophy (FSHD) is caused by the mis-expression of DUX4 in skeletal muscle cells. DUX4 is a transcription factor that activates genes normally associated with stem cell biology and its mis-expression in FSHD cells results in apoptosis. To identify genes and pathways necessary for DUX4-mediated apoptosis, we performed an siRNA screen in an RD rhabdomyosarcoma cell line with an inducible DUX4 transgene. Our screen identified components of the MYC-mediated apoptotic pathway and the double-stranded RNA (dsRNA) innate immune response pathway as mediators of DUX4-induced apoptosis. Further investigation revealed that DUX4 expression led to increased MYC mRNA, accumulation of nuclear dsRNA foci, and activation of the dsRNA response pathway in both RD cells and human myoblasts. Nuclear dsRNA foci were associated with aggregation of the exon junction complex component EIF4A3. The elevation of MYC mRNA, dsRNA accumulation, and EIF4A3 nuclear aggregates in FSHD muscle cells suggest that these processes might contribute to FSHD pathophysiology.
    MeSH term(s) Apoptosis ; Caspases/metabolism ; Cell Death ; Cell Line ; Cell Survival ; DEAD-box RNA Helicases/genetics ; Eukaryotic Initiation Factor-4A/genetics ; Exons ; Gene Expression Regulation ; Homeodomain Proteins/genetics ; Humans ; Immunity, Innate ; Muscular Dystrophy, Facioscapulohumeral/genetics ; Muscular Dystrophy, Facioscapulohumeral/pathology ; Mutation ; Myoblasts/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; RNA, Double-Stranded/genetics ; RNA, Double-Stranded/metabolism ; RNA, Messenger/metabolism ; RNA, Small Interfering/metabolism ; Rhabdomyosarcoma/genetics ; Tumor Suppressor Protein p53/genetics
    Chemical Substances DUX4L1 protein, human ; Homeodomain Proteins ; MYC protein, human ; Proto-Oncogene Proteins c-myc ; RNA, Double-Stranded ; RNA, Messenger ; RNA, Small Interfering ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Eukaryotic Initiation Factor-4A (EC 2.7.7.-) ; Caspases (EC 3.4.22.-) ; EIF4A3 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Language English
    Publishing date 2017-03-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1006658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Changes in H2A.Z occupancy and DNA methylation during B-cell lymphomagenesis.

    Conerly, Melissa L / Teves, Sheila S / Diolaiti, Daniel / Ulrich, Michelle / Eisenman, Robert N / Henikoff, Steven

    Genome research

    2010  Volume 20, Issue 10, Page(s) 1383–1390

    Abstract: The histone variant H2A.Z has been implicated in the regulation of gene expression, and in plants antagonizes DNA methylation. Here, we ask whether a similar relationship exists in mammals, using a mouse B-cell lymphoma model, where chromatin states can ... ...

    Abstract The histone variant H2A.Z has been implicated in the regulation of gene expression, and in plants antagonizes DNA methylation. Here, we ask whether a similar relationship exists in mammals, using a mouse B-cell lymphoma model, where chromatin states can be monitored during tumorigenesis. Using native chromatin immunoprecipitation with microarray hybridization (ChIP-chip), we found a progressive depletion of H2A.Z around transcriptional start sites (TSSs) during MYC-induced transformation of pre-B cells and, subsequently, during lymphomagenesis. In addition, we found that H2A.Z and DNA methylation are generally anticorrelated around TSSs in both wild-type and MYC-transformed cells, as expected for the opposite effects of these chromatin features on promoter competence. Depletion of H2A.Z over TSSs both in cells that are induced to proliferate and in cells that are developing into a tumor suggests that progressive loss of H2A.Z during tumorigenesis results from the advancing disease state. These changes were accompanied by increases in chromatin salt solubility. Surprisingly, ∼30% of all genes showed a redistribution of H2A.Z from around TSSs to bodies of active genes during the transition from MYC-transformed to tumor cells, with DNA methylation lost from gene bodies where H2A.Z levels increased. No such redistributions were observed during MYC-induced transformation of wild-type pre-B cells. The documented role of H2A.Z in regulating transcription suggests that 30% of genes have the potential to be aberrantly expressed during tumorigenesis. Our results imply that antagonism between H2A.Z deposition and DNA methylation is a conserved feature of eukaryotic genes, and that transcription-coupled H2A.Z changes may play a role in cancer initiation and progression.
    MeSH term(s) Animals ; Animals, Genetically Modified ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Cell Transformation, Neoplastic ; Chromatin Immunoprecipitation ; DNA Methylation ; Disease Models, Animal ; Female ; Gene Expression Regulation, Neoplastic ; Histones/metabolism ; Lymphoma, B-Cell/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Nucleic Acid Hybridization ; Precursor Cells, B-Lymphoid/metabolism ; Precursor Cells, B-Lymphoid/pathology
    Chemical Substances Histones
    Language English
    Publishing date 2010-08-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1284872-4
    ISSN 1549-5469 ; 1088-9051 ; 1054-9803
    ISSN (online) 1549-5469
    ISSN 1088-9051 ; 1054-9803
    DOI 10.1101/gr.106542.110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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