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4. Comparative analysis of regulatory elements of the Myf-5 gene

Author

Coutelle, Oliver

Subjects
591.35
Abstract

The work presented here addresses the question of how skeletal muscle formation is initiated in the mouse by dissecting the regulatory mechanisms that control the myogenic regulatory factor Myf-5. Myf-5 is expressed in the dorsal somite from E8, before the other MRFs, myogenin, MRF4 and MyoD, become activated. In the mouse Myf-5 is located 8.5kb downstream of MRF4. Previous results have shown that dispersed over the intergenic region and intragenic regions are the regulatory elements involved in directing Myf-5 expression to the different anatomical subdomains that make up its complete expression pattern. The regulatory element(s) controlling the dorsal somite expression of Myf-5 is contained in the intergenic region while ventral somite expression depends on elements in the Myf-5 gene itself. Because of the large size of this region I have isolated the MRF4 and Myf-5 genes of the teleost Fugu rubripes, which has a genome eight times smaller than that of the mouse. Although synteny is conserved in Fugu and the intergenic distance is only 3kb, noncoding sequence including the introns is poorly conserved. Focusing on the Myf-5 gene itself, sequence comparison between the mouse and human Myf-5 genes was employed sucessfully to eliminate more than 60% of the intron sequence by identifying conserved regions in the 3'half of each of the Myf-5 introns which, together with the 3'UTR can activate reporter gene expression in the ventral posterior part of the somites. EMSA analysis with embryonic protein extracts revealed several protein binding regions within the conserved intron fragments and subsequent transgenic analysis showed not only that separate genomic regions control individual anatomical domains of Myf-5 expression, but that within these regions multiple binding sites are found, adding a further level of complexity to the regulation of Myf-5. Analysis of the Fugu Myf-5 gene in transgenic mice showed remarkable similarities with the expression pattern of Myf-5 in another teleost, the zebrafish Danio rerio. Both are expressed in the presomitic mesoderm, as well as the somites, suggesting that the expression of the Fugu transgene is a reflection of its native expression pattern.

Published
1998

8. Tumour-infiltrating neutrophils counteract anti-VEGF therapy in metastatic colorectal cancer

Author

Schiffmann, Lars Mortimer, primary, Fritsch, Melanie, additional, Gebauer, Florian, additional, Günther, Saskia Diana, additional, Stair, Neil Richard, additional, Seeger, Jens Michael, additional, Thangarajah, Fabinshy, additional, Dieplinger, Georg, additional, Bludau, Marc, additional, Alakus, Hakan, additional, Göbel, Heike, additional, Quaas, Alexander, additional, Zander, Thomas, additional, Hilberg, Frank, additional, Bruns, Christiane Josephine, additional, Kashkar, Hamid, additional, and Coutelle, Oliver, additional

Published
2018
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10. Hedgehog Signalling Is Required for Maintenance of myf5 and myoD Expression and Timely Terminal Differentiation in Zebrafish Adaxial Myogenesis

Author

Coutelle, Oliver, Blagden, Chris S., Hampson, Richard, Halai, Chandi, Rigby, Peter W. J., and Hughes, Simon M.

Subjects
Zebra fish -- Genetic aspects, Myogenesis -- Research, Biological sciences
Abstract

Hedgehog proteins have been implicated in the control of myogenesis in the medial vertebrate somite. In the mouse, normal epaxial expression of the myogenic transcription factor gene myf5 is dependent on Sonic hedgehog. Here we examine in zebrafish the interaction between Hedgehog signals, the expression of myoD family genes, including the newly cloned zebrafish myf5, and slow myogenesis. We show that Sonic hedgehog is necessary for normal expression of both myf5 and myoD in adaxial slow muscle precursors, but not in lateral paraxial mesoderm. Expression of both genes is initiated normally in rostral presomitic mesoderm in sonic you mutants, which lack all Sonic hedgehog. Similar initiation continues during tailbud outgrowth when the cells forming caudal somites are generated. However, adaxial cells in sonic you embryos are delayed in terminal differentiation and caudal adaxial cells fail to maintain myogenic regulatory factor expression. Despite these defects, other signals are able to maintain, or reinitiate, some slow muscle development in sonic you mutants. In the cyclops mutant, the absence of floorplate-derived Tiggywinkle hedgehog and Sonic hedgehog has no discernible effect on slow adaxial myogenesis. Similarly, the absence of notochord-derived Sonic hedgehog and Echidna hedgehog in mutants lacking notochord delays, but does not prevent, adaxial slow muscle development. In contrast, removal of both Sonic hedgehog and a floorplate signal, probably Tiggywinkle hedgehog, from the embryonic midline in cyclops;sonic you double mutants essentially abolishes slow myogenesis. We conclude that several midline signals, likely to be various Hedgehogs, collaborate to maintain adaxial slow myogenesis in the zebrafish embryo. Moreover, the data demonstrate that, in the absence of this required Hedgehog signalling, expression of myf5 and myoD is insufficient to commit cells to adaxial myogenesis. Key Words: skeletal muscle; zebrafish; myf5; myoD; hedgehog; differentiation; somite; myoblast; myogenesis.

Published
2001

12. IAP antagonization promotes inflammatory destruction of vascular endothelium

Author

Witt, Axel, primary, Seeger, Jens M, additional, Coutelle, Oliver, additional, Zigrino, Paola, additional, Broxtermann, Pia, additional, Andree, Maria, additional, Brinkmann, Kerstin, additional, Jüngst, Christian, additional, Schauss, Astrid C, additional, Schüll, Stephan, additional, Wohlleber, Dirk, additional, Knolle, Percy A, additional, Krönke, Martin, additional, Mauch, Cornelia, additional, and Kashkar, Hamid, additional

Published
2015
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14. BID ‐dependent release of mitochondrial SMAC dampens XIAP ‐mediated immunity against Shigella

Author

Andree, Maria, primary, Seeger, Jens M, additional, Schüll, Stephan, additional, Coutelle, Oliver, additional, Wagner‐Stippich, Diana, additional, Wiegmann, Katja, additional, Wunderlich, Claudia M, additional, Brinkmann, Kerstin, additional, Broxtermann, Pia, additional, Witt, Axel, additional, Fritsch, Melanie, additional, Martinelli, Paola, additional, Bielig, Harald, additional, Lamkemeyer, Tobias, additional, Rugarli, Elena I, additional, Kaufmann, Thomas, additional, Sterner‐Kock, Anja, additional, Wunderlich, F Thomas, additional, Villunger, Andreas, additional, Martins, L Miguel, additional, Krönke, Martin, additional, Kufer, Thomas A, additional, Utermöhlen, Olaf, additional, and Kashkar, Hamid, additional

Published
2014
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15. Ubiquitin C-Terminal Hydrolase-L1 Potentiates Cancer Chemosensitivity by Stabilizing NOXA

Author

Brinkmann, Kerstin, primary, Zigrino, Paola, additional, Witt, Axel, additional, Schell, Michael, additional, Ackermann, Leena, additional, Broxtermann, Pia, additional, Schüll, Stephan, additional, Andree, Maria, additional, Coutelle, Oliver, additional, Yazdanpanah, Benjamin, additional, Seeger, Jens Michael, additional, Klubertz, Daniela, additional, Drebber, Uta, additional, Hacker, Ulrich T., additional, Krönke, Martin, additional, Mauch, Cornelia, additional, Hoppe, Thorsten, additional, and Kashkar, Hamid, additional

Published
2013
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17. Hepatocyte Growth Factor (HGF) Inhibits Collagen I and IV Synthesis in Hepatic Stellate Cells by miRNA-29 Induction

Author

Kwiecinski, Monika, primary, Noetel, Andrea, additional, Elfimova, Natalia, additional, Trebicka, Jonel, additional, Schievenbusch, Stephanie, additional, Strack, Ingo, additional, Molnar, Levente, additional, von Brandenstein, Melanie, additional, Töx, Ulrich, additional, Nischt, Roswitha, additional, Coutelle, Oliver, additional, Dienes, Hans Peter, additional, and Odenthal, Margarete, additional

Published
2011
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19. Combined Paracrine and Endocrine AAV9 mediated Expression of Hepatocyte Growth Factor for the Treatment of Renal Fibrosis

Author

Schievenbusch, Stephanie, primary, Strack, Ingo, additional, Scheffler, Melanie, additional, Nischt, Roswitha, additional, Coutelle, Oliver, additional, Hösel, Marianna, additional, Hallek, Michael, additional, Fries, Jochen WU, additional, Dienes, Hans-Peter, additional, Odenthal, Margarete, additional, and Büning, Hildegard, additional

Published
2010
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24. Recent developments in adeno-associated virus vector technology.

Author

Büning, Hildegard, Perabo, Luca, Coutelle, Oliver, Quadt-Humme, Sibille, and Hallek, Michael

Abstract

Adeno-associated virus (AAV), a single-stranded DNA parvovirus, is emerging as one of the leading gene therapy vectors owing to its nonpathogenicity and low immunogenicity, stability and the potential to integrate site-specifically without known side-effects. A portfolio of recombinant AAV vector types has been developed with the aim of optimizing efficiency, specificity and thereby also the safety of in vitro and in vivo gene transfer. More and more information is now becoming available about the mechanism of AAV/host cell interaction improving the efficacy of recombinant AAV vector (rAAV) mediated gene delivery. This review summarizes the current knowledge of the infectious biology of AAV, provides an overview of the latest developments in the field of AAV vector technology and discusses remaining challenges. Copyright © 2008 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2008
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25. Hedgehog Signalling Is Required for Maintenance of myf5and myoDExpression and Timely Terminal Differentiation in Zebrafish Adaxial Myogenesis

Author

Coutelle, Oliver, Blagden, Chris S., Hampson, Richard, Halai, Chandi, Rigby, Peter W.J., and Hughes, Simon M.

Abstract

Hedgehog proteins have been implicated in the control of myogenesis in the medial vertebrate somite. In the mouse, normal epaxial expression of the myogenic transcription factor gene myf5is dependent on Sonic hedgehog. Here we examine in zebrafish the interaction between Hedgehog signals, the expression of myoDfamily genes, including the newly cloned zebrafish myf5,and slow myogenesis. We show that Sonic hedgehog is necessary for normal expression of both myf5and myoDin adaxial slow muscle precursors, but not in lateral paraxial mesoderm. Expression of both genes is initiated normally in rostral presomitic mesoderm in sonic youmutants, which lack all Sonic hedgehog. Similar initiation continues during tailbud outgrowth when the cells forming caudal somites are generated. However, adaxial cells in sonic youembryos are delayed in terminal differentiation and caudal adaxial cells fail to maintain myogenic regulatory factor expression. Despite these defects, other signals are able to maintain, or reinitiate, some slow muscle development in sonic youmutants. In the cyclopsmutant, the absence of floorplate-derived Tiggywinkle hedgehog and Sonic hedgehog has no discernible effect on slow adaxial myogenesis. Similarly, the absence of notochord-derived Sonic hedgehog and Echidna hedgehog in mutants lacking notochord delays, but does not prevent, adaxial slow muscle development. In contrast, removal of both Sonic hedgehog and a floorplate signal, probably Tiggywinkle hedgehog, from the embryonic midline in cyclops;sonic youdouble mutants essentially abolishes slow myogenesis. We conclude that several midline signals, likely to be various Hedgehogs, collaborate to maintain adaxial slow myogenesis in the zebrafish embryo. Moreover, the data demonstrate that, in the absence of this required Hedgehog signalling, expression of myf5and myoDis insufficient to commit cells to adaxial myogenesis.

Published
2001
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26. The expression of Myf5 in the developing mouse embryo is controlled by discrete and dispersed enhancers specific for particular populations of skeletal muscle precursors

Author

Summerbell, Dennis, Ashby, Peter R., Coutelle, Oliver, Cox, David, Yee, Siu-Pok, and Rigby, Peter W. J.

Abstract

The development of skeletal muscle in vertebrate embryos is controlled by a transcriptional cascade that includes the four myogenic regulatory factors Myf5, Myogenin, MRF4 and MyoD. In the mouse embryo, Myf5 is the first of these factors to be expressed and mutational analyses suggest that this protein acts early in the process of commitment to the skeletal muscle fate. We have therefore analysed the regulation of Myf5 gene expression using transgenic technology and find that its control is markedly different from that of the other two myogenic regulatory factor genes previously analysed, Myogenin and MyoD. We show that Myf5 is regulated through a number of distinct and discrete enhancers, dispersed throughout 14 kb spanning the MRF4/Myf5 locus, each of which drives reporter gene expression in a particular subset of skeletal muscle precursors. This region includes four separate enhancers controlling expression in the epaxial muscle precursors of the body, some hypaxial precursors of the body, some facial muscles and the central nervous system. These elements separately or together are unable to drive expression in the cells that migrate to the limb buds and in some other muscle subsets and to correctly maintain expression at late times. We suggest that this complex mechanism of control has evolved because different inductive signals operate in each population of muscle precursors and thus distinct enhancers, and cognate transcription factors, are required to interpret them.

Published
2000
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