Antagonism between Smad1 and Smad2 signaling determines the site of distal visceral endoderm formation in the mouse embryo
The anterior-posterior axis of the mouse embryo is established by formation of distal visceral endoderm (DVE) and its subsequent migration. The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE forma...
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| Veröffentlicht in: | The Journal of cell biology 2009-01, Vol.184 (2), p.323-334 |
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| container_title | The Journal of cell biology |
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| creator | Yamamoto, Masamichi Beppu, Hideyuki Takaoka, Katsuyoshi Meno, Chikara Li, En Miyazono, Kohei Hamada, Hiroshi |
| description | The anterior-posterior axis of the mouse embryo is established by formation of distal visceral endoderm (DVE) and its subsequent migration. The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE formation. BMP signaling is required at an early stage for differentiation of the primitive endoderm into the embryonic visceral endoderm (VE), whereas it inhibits DVE formation, restricting it to the distal region, at a later stage. A Smad2-activating factor such as Activin also contributes to DVE formation by generating a region of VE positive for the Smad2 signal and negative for Smad1 signal. DVE is thus formed at the distal end of the embryo, the only region of VE negative for the Smad1 signal and positive for Smad2 signal. An inverse relation between the level of phosphorylated Smad1 and that of phosphorylated Smad2 in VE suggests an involvement of antagonism between Smad1- and Smad2-mediated signaling. |
| doi_str_mv | 10.1083/jcb.200808044 |
| format | Article |
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The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE formation. BMP signaling is required at an early stage for differentiation of the primitive endoderm into the embryonic visceral endoderm (VE), whereas it inhibits DVE formation, restricting it to the distal region, at a later stage. A Smad2-activating factor such as Activin also contributes to DVE formation by generating a region of VE positive for the Smad2 signal and negative for Smad1 signal. DVE is thus formed at the distal end of the embryo, the only region of VE negative for the Smad1 signal and positive for Smad2 signal. An inverse relation between the level of phosphorylated Smad1 and that of phosphorylated Smad2 in VE suggests an involvement of antagonism between Smad1- and Smad2-mediated signaling.</description><identifier>ISSN: 0021-9525</identifier><identifier>EISSN: 1540-8140</identifier><identifier>DOI: 10.1083/jcb.200808044</identifier><identifier>PMID: 19153222</identifier><identifier>CODEN: JCLBA3</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Antibodies ; Binding sites ; Body Patterning - genetics ; Cell adhesion & migration ; Cells ; Developmental biology ; Embryo, Mammalian - metabolism ; Embryonic stem cells ; Embryos ; Endoderm ; Endoderm - metabolism ; Female ; Gene Expression Regulation, Developmental ; Germ cells ; In situ hybridization ; Mice ; Mice, Transgenic ; Pregnancy ; Receptors ; Rodents ; Signal Transduction - genetics ; Smad1 Protein - metabolism ; Smad2 Protein - metabolism ; Stem cells ; Tetraploidy</subject><ispartof>The Journal of cell biology, 2009-01, Vol.184 (2), p.323-334</ispartof><rights>Copyright Rockefeller University Press Jan 28, 2009</rights><rights>2009 Yamamoto et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-1a9c2aa01ef68545ce738f89d21a39827e7c2ec68545883cbcd821b46be011433</citedby><cites>FETCH-LOGICAL-c524t-1a9c2aa01ef68545ce738f89d21a39827e7c2ec68545883cbcd821b46be011433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19153222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamamoto, Masamichi</creatorcontrib><creatorcontrib>Beppu, Hideyuki</creatorcontrib><creatorcontrib>Takaoka, Katsuyoshi</creatorcontrib><creatorcontrib>Meno, Chikara</creatorcontrib><creatorcontrib>Li, En</creatorcontrib><creatorcontrib>Miyazono, Kohei</creatorcontrib><creatorcontrib>Hamada, Hiroshi</creatorcontrib><title>Antagonism between Smad1 and Smad2 signaling determines the site of distal visceral endoderm formation in the mouse embryo</title><title>The Journal of cell biology</title><addtitle>J Cell Biol</addtitle><description>The anterior-posterior axis of the mouse embryo is established by formation of distal visceral endoderm (DVE) and its subsequent migration. The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE formation. BMP signaling is required at an early stage for differentiation of the primitive endoderm into the embryonic visceral endoderm (VE), whereas it inhibits DVE formation, restricting it to the distal region, at a later stage. A Smad2-activating factor such as Activin also contributes to DVE formation by generating a region of VE positive for the Smad2 signal and negative for Smad1 signal. DVE is thus formed at the distal end of the embryo, the only region of VE negative for the Smad1 signal and positive for Smad2 signal. 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Beppu, Hideyuki ; Takaoka, Katsuyoshi ; Meno, Chikara ; Li, En ; Miyazono, Kohei ; Hamada, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-1a9c2aa01ef68545ce738f89d21a39827e7c2ec68545883cbcd821b46be011433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Binding sites</topic><topic>Body Patterning - genetics</topic><topic>Cell adhesion & migration</topic><topic>Cells</topic><topic>Developmental biology</topic><topic>Embryo, Mammalian - metabolism</topic><topic>Embryonic stem cells</topic><topic>Embryos</topic><topic>Endoderm</topic><topic>Endoderm - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Germ cells</topic><topic>In situ hybridization</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Pregnancy</topic><topic>Receptors</topic><topic>Rodents</topic><topic>Signal Transduction - genetics</topic><topic>Smad1 Protein - metabolism</topic><topic>Smad2 Protein - metabolism</topic><topic>Stem cells</topic><topic>Tetraploidy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamamoto, Masamichi</creatorcontrib><creatorcontrib>Beppu, Hideyuki</creatorcontrib><creatorcontrib>Takaoka, Katsuyoshi</creatorcontrib><creatorcontrib>Meno, Chikara</creatorcontrib><creatorcontrib>Li, En</creatorcontrib><creatorcontrib>Miyazono, Kohei</creatorcontrib><creatorcontrib>Hamada, Hiroshi</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamamoto, Masamichi</au><au>Beppu, Hideyuki</au><au>Takaoka, Katsuyoshi</au><au>Meno, Chikara</au><au>Li, En</au><au>Miyazono, Kohei</au><au>Hamada, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antagonism between Smad1 and Smad2 signaling determines the site of distal visceral endoderm formation in the mouse embryo</atitle><jtitle>The Journal of cell biology</jtitle><addtitle>J Cell Biol</addtitle><date>2009-01-26</date><risdate>2009</risdate><volume>184</volume><issue>2</issue><spage>323</spage><epage>334</epage><pages>323-334</pages><issn>0021-9525</issn><eissn>1540-8140</eissn><coden>JCLBA3</coden><abstract>The anterior-posterior axis of the mouse embryo is established by formation of distal visceral endoderm (DVE) and its subsequent migration. The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE formation. BMP signaling is required at an early stage for differentiation of the primitive endoderm into the embryonic visceral endoderm (VE), whereas it inhibits DVE formation, restricting it to the distal region, at a later stage. A Smad2-activating factor such as Activin also contributes to DVE formation by generating a region of VE positive for the Smad2 signal and negative for Smad1 signal. DVE is thus formed at the distal end of the embryo, the only region of VE negative for the Smad1 signal and positive for Smad2 signal. 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| subjects | Animals Antibodies Binding sites Body Patterning - genetics Cell adhesion & migration Cells Developmental biology Embryo, Mammalian - metabolism Embryonic stem cells Embryos Endoderm Endoderm - metabolism Female Gene Expression Regulation, Developmental Germ cells In situ hybridization Mice Mice, Transgenic Pregnancy Receptors Rodents Signal Transduction - genetics Smad1 Protein - metabolism Smad2 Protein - metabolism Stem cells Tetraploidy |
| title | Antagonism between Smad1 and Smad2 signaling determines the site of distal visceral endoderm formation in the mouse embryo |
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