Megf10 regulates the progression of the satellite cell myogenic program
We identify here the multiple epidermal growth factor repeat transmembrane protein Megf10 as a quiescent satellite cell marker that is also expressed in skeletal myoblasts but not in differentiated myofibers. Retroviral expression of Megf10 in myoblasts results in enhanced proliferation and inhibite...
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| Veröffentlicht in: | The Journal of cell biology 2007-12, Vol.179 (5), p.911-922 |
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| container_title | The Journal of cell biology |
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| creator | Holterman, Chet E Le Grand, Fabien Kuang, Shihuan Seale, Patrick Rudnicki, Michael A |
| description | We identify here the multiple epidermal growth factor repeat transmembrane protein Megf10 as a quiescent satellite cell marker that is also expressed in skeletal myoblasts but not in differentiated myofibers. Retroviral expression of Megf10 in myoblasts results in enhanced proliferation and inhibited differentiation. Infected myoblasts that fail to differentiate undergo cell cycle arrest and can reenter the cell cycle upon serum restimulation. Moreover, experimental modulations of Megf10 alter the expression levels of Pax7 and the myogenic regulatory factors. In contrast, Megf10 silencing in activated satellite cells on individual fibers or in cultured myoblasts results in a dramatic reduction in the cell number, caused by myogenin activation and precocious differentiation as well as a depletion of the self-renewing Pax7⁺/MyoD⁻ population. Additionally, Megf10 silencing in MyoD⁻/⁻ myoblasts results in down-regulation of Notch signaling components. We conclude that Megf10 represents a novel transmembrane protein that impinges on Notch signaling to regulate the satellite cell population balance between proliferation and differentiation. |
| doi_str_mv | 10.1083/jcb.200709083 |
| format | Article |
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Retroviral expression of Megf10 in myoblasts results in enhanced proliferation and inhibited differentiation. Infected myoblasts that fail to differentiate undergo cell cycle arrest and can reenter the cell cycle upon serum restimulation. Moreover, experimental modulations of Megf10 alter the expression levels of Pax7 and the myogenic regulatory factors. In contrast, Megf10 silencing in activated satellite cells on individual fibers or in cultured myoblasts results in a dramatic reduction in the cell number, caused by myogenin activation and precocious differentiation as well as a depletion of the self-renewing Pax7⁺/MyoD⁻ population. Additionally, Megf10 silencing in MyoD⁻/⁻ myoblasts results in down-regulation of Notch signaling components. We conclude that Megf10 represents a novel transmembrane protein that impinges on Notch signaling to regulate the satellite cell population balance between proliferation and differentiation.</description><identifier>ISSN: 0021-9525</identifier><identifier>EISSN: 1540-8140</identifier><identifier>DOI: 10.1083/jcb.200709083</identifier><identifier>PMID: 18056409</identifier><identifier>CODEN: JCLBA3</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Artificial satellites ; Cell Compartmentation ; Cell culture ; Cell cycle ; Cell Differentiation ; Cell growth ; Cell Proliferation ; Cellular differentiation ; DNA, Complementary - isolation & purification ; Down regulation ; Gene expression ; Hepatocytes ; Membrane Proteins - deficiency ; Membrane Proteins - metabolism ; Mice ; Muscle Development ; Muscle, Skeletal - cytology ; Muscle, Skeletal - metabolism ; Myoblasts ; Proteins ; Receptors, Notch - metabolism ; Satellite Cells, Skeletal Muscle - cytology ; Serum ; Signal Transduction ; Skeletal muscle ; Skeletal muscle satellite cells ; Stem cells ; Stem Cells - cytology ; Stem Cells - metabolism</subject><ispartof>The Journal of cell biology, 2007-12, Vol.179 (5), p.911-922</ispartof><rights>Copyright 2007 The Rockefeller University Press</rights><rights>Copyright Rockefeller University Press Dec 3, 2007</rights><rights>Copyright © 2007, The Rockefeller University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c555t-30f3bd0e61ad56a10601b20fa9c7200e076f228d45a67df97d1804fa5a785b643</citedby><cites>FETCH-LOGICAL-c555t-30f3bd0e61ad56a10601b20fa9c7200e076f228d45a67df97d1804fa5a785b643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18056409$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Holterman, Chet E</creatorcontrib><creatorcontrib>Le Grand, Fabien</creatorcontrib><creatorcontrib>Kuang, Shihuan</creatorcontrib><creatorcontrib>Seale, Patrick</creatorcontrib><creatorcontrib>Rudnicki, Michael A</creatorcontrib><title>Megf10 regulates the progression of the satellite cell myogenic program</title><title>The Journal of cell biology</title><addtitle>J Cell Biol</addtitle><description>We identify here the multiple epidermal growth factor repeat transmembrane protein Megf10 as a quiescent satellite cell marker that is also expressed in skeletal myoblasts but not in differentiated myofibers. Retroviral expression of Megf10 in myoblasts results in enhanced proliferation and inhibited differentiation. Infected myoblasts that fail to differentiate undergo cell cycle arrest and can reenter the cell cycle upon serum restimulation. Moreover, experimental modulations of Megf10 alter the expression levels of Pax7 and the myogenic regulatory factors. In contrast, Megf10 silencing in activated satellite cells on individual fibers or in cultured myoblasts results in a dramatic reduction in the cell number, caused by myogenin activation and precocious differentiation as well as a depletion of the self-renewing Pax7⁺/MyoD⁻ population. Additionally, Megf10 silencing in MyoD⁻/⁻ myoblasts results in down-regulation of Notch signaling components. 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Retroviral expression of Megf10 in myoblasts results in enhanced proliferation and inhibited differentiation. Infected myoblasts that fail to differentiate undergo cell cycle arrest and can reenter the cell cycle upon serum restimulation. Moreover, experimental modulations of Megf10 alter the expression levels of Pax7 and the myogenic regulatory factors. In contrast, Megf10 silencing in activated satellite cells on individual fibers or in cultured myoblasts results in a dramatic reduction in the cell number, caused by myogenin activation and precocious differentiation as well as a depletion of the self-renewing Pax7⁺/MyoD⁻ population. Additionally, Megf10 silencing in MyoD⁻/⁻ myoblasts results in down-regulation of Notch signaling components. 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| subjects | Animals Artificial satellites Cell Compartmentation Cell culture Cell cycle Cell Differentiation Cell growth Cell Proliferation Cellular differentiation DNA, Complementary - isolation & purification Down regulation Gene expression Hepatocytes Membrane Proteins - deficiency Membrane Proteins - metabolism Mice Muscle Development Muscle, Skeletal - cytology Muscle, Skeletal - metabolism Myoblasts Proteins Receptors, Notch - metabolism Satellite Cells, Skeletal Muscle - cytology Serum Signal Transduction Skeletal muscle Skeletal muscle satellite cells Stem cells Stem Cells - cytology Stem Cells - metabolism |
| title | Megf10 regulates the progression of the satellite cell myogenic program |
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