Twist controls skeletal development and dorsoventral patterning by regulating runx2 in zebrafish
Twist1a and twist1b are the principal components of twists that negatively regulate a number of cellular signaling events. Expression of runx2 and downstream targets is essential for skeletal development and ventral organizer formation and specification in early vertebrate embryos, but what controls...
Gespeichert in:
| Veröffentlicht in: | PloS one 2011-11, Vol.6 (11), p.e27324-e27324 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e27324 |
|---|---|
| container_issue | 11 |
| container_start_page | e27324 |
| container_title | PloS one |
| container_volume | 6 |
| creator | Yang, Der-Chih Tsai, Chih-Chien Liao, Yun-Feng Fu, Hui-Chuan Tsay, Huey-Jen Huang, Tung-Fu Chen, Yau-Hung Hung, Shih-Chieh |
| description | Twist1a and twist1b are the principal components of twists that negatively regulate a number of cellular signaling events. Expression of runx2 and downstream targets is essential for skeletal development and ventral organizer formation and specification in early vertebrate embryos, but what controls ventral activity of maternal runx2 and how twists function in zebrafish embryogenesis still remain unclear.
By studying the loss of twist induced by injection of morpholino-oligonucleotide in zebrafish, we found that twist1a and twist1b, but not twist2 or twist3, were required for proper skeletal development and dorsoventral patterning in early embryos. Overexpression of twist1a or twist1b following mRNA injection resulted in deteriorated skeletal development and formation of typical dorsalized embryos, whereas knockdown of twist1a and twist1b led to the formation of abnormal embryos with enhanced skeletal formation and typical ventralized patterning. Overexpression of twist1a or twist1b decreased the expression of runx2b, whereas twist1a and twist1b knockdown increased runx2b expression. We have further demonstrated that phenotypes induced by twist1a and twist1b knockdown were rescued by runx2b knockdown.
Together, these results suggest that twist1a and twist1b control skeletal development and dorsoventral patterning by regulating runx2b in zebrafish and provide potential targets for the treatment of diseases or syndromes associated with decreased skeletal development. |
| doi_str_mv | 10.1371/journal.pone.0027324 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1310659350</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A476863358</galeid><doaj_id>oai_doaj_org_article_4aaeea9ea4404543ae9092818b8e1d13</doaj_id><sourcerecordid>A476863358</sourcerecordid><originalsourceid>FETCH-LOGICAL-c691t-b609c95a66666a766abaf08c57532ef5315b64a6395688747bf6583cf95e1c423</originalsourceid><addsrcrecordid>eNqNk11v0zAUhiMEYqPwDxBEQgJx0eKP2IlvkKaJj0qTJsHg1jjJSeri2p3tjI1fj0uzqUG7IFaU2H7Oa_v1OVn2HKMFpiV-t3aDt8osts7CAiFSUlI8yI6xoGTOCaIPD_6PsichrBFitOL8cXZECKpKIvBx9uPilw4xb5yN3pmQh59gICqTt3AFxm03YGOubJu3zgd3lXo-TW5VjOCttn1e3-Qe-sGouOv5wV6TXNv8N9RedTqsnmaPOmUCPBu_s-zbxw8Xp5_nZ-eflqcnZ_OGCxznNUeiEUzx3aPK9NaqQ1XDSkYJdIxiVvNCcSoYr6qyKOuOs4o2nWCAm4LQWfZyr7s1LsjRnCAxxYgzQRlKxHJPtE6t5dbrjfI30ikt_w4430vlo24MyEIpACVAFQUqWEEVCCRIhau6AtximrTej6sN9QbaZu_LRHQ6Y_VK9u5KUoIRTvuZZW9GAe8uBwhRbnRowBhlwQ1BCsR4idNFJ_LVP-T9hxupXqX9a9u5tGyz05QnRckrTmmya5Yt7qFSa2GjUw5Ap9P4JODtJGCXJ3AdezWEIJdfv_w_e_59yr4-YFegTFwFZ4aonQ1TsNiDjXcheOjuPMZI7urg1g25qwM51kEKe3F4P3dBt4lP_wCHYgMp</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1310659350</pqid></control><display><type>article</type><title>Twist controls skeletal development and dorsoventral patterning by regulating runx2 in zebrafish</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Yang, Der-Chih ; Tsai, Chih-Chien ; Liao, Yun-Feng ; Fu, Hui-Chuan ; Tsay, Huey-Jen ; Huang, Tung-Fu ; Chen, Yau-Hung ; Hung, Shih-Chieh</creator><contributor>Milstone, David S.</contributor><creatorcontrib>Yang, Der-Chih ; Tsai, Chih-Chien ; Liao, Yun-Feng ; Fu, Hui-Chuan ; Tsay, Huey-Jen ; Huang, Tung-Fu ; Chen, Yau-Hung ; Hung, Shih-Chieh ; Milstone, David S.</creatorcontrib><description>Twist1a and twist1b are the principal components of twists that negatively regulate a number of cellular signaling events. Expression of runx2 and downstream targets is essential for skeletal development and ventral organizer formation and specification in early vertebrate embryos, but what controls ventral activity of maternal runx2 and how twists function in zebrafish embryogenesis still remain unclear.
By studying the loss of twist induced by injection of morpholino-oligonucleotide in zebrafish, we found that twist1a and twist1b, but not twist2 or twist3, were required for proper skeletal development and dorsoventral patterning in early embryos. Overexpression of twist1a or twist1b following mRNA injection resulted in deteriorated skeletal development and formation of typical dorsalized embryos, whereas knockdown of twist1a and twist1b led to the formation of abnormal embryos with enhanced skeletal formation and typical ventralized patterning. Overexpression of twist1a or twist1b decreased the expression of runx2b, whereas twist1a and twist1b knockdown increased runx2b expression. We have further demonstrated that phenotypes induced by twist1a and twist1b knockdown were rescued by runx2b knockdown.
Together, these results suggest that twist1a and twist1b control skeletal development and dorsoventral patterning by regulating runx2b in zebrafish and provide potential targets for the treatment of diseases or syndromes associated with decreased skeletal development.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0027324</identifier><identifier>PMID: 22087291</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Basic Helix-Loop-Helix Transcription Factors - physiology ; Biology ; Body Patterning - genetics ; Bone Development - genetics ; Cancer ; Cbfa-1 protein ; Clinical medicine ; Danio rerio ; Drosophila ; Education ; Embryogenesis ; Embryonic development ; Embryonic Development - genetics ; Embryonic growth stage ; Embryos ; Epidemiology ; Gene expression ; Gene Expression Regulation, Developmental ; Genomes ; Hospitals ; Hypoxia ; Injection ; Insects ; Mammals ; Medical research ; Medical treatment ; Mineralization ; mRNA ; Neurosciences ; Oligonucleotides ; Pattern formation ; Proteins ; RNA ; Signaling ; Studies ; Therapeutics ; Transcription factors ; Transcription Factors - deficiency ; Transcription Factors - genetics ; Transcription Factors - physiology ; Zebrafish ; Zebrafish - embryology ; Zebrafish - genetics ; Zebrafish Proteins - deficiency ; Zebrafish Proteins - genetics ; Zebrafish Proteins - physiology</subject><ispartof>PloS one, 2011-11, Vol.6 (11), p.e27324-e27324</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Yang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Yang et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-b609c95a66666a766abaf08c57532ef5315b64a6395688747bf6583cf95e1c423</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210159/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210159/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22087291$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Milstone, David S.</contributor><creatorcontrib>Yang, Der-Chih</creatorcontrib><creatorcontrib>Tsai, Chih-Chien</creatorcontrib><creatorcontrib>Liao, Yun-Feng</creatorcontrib><creatorcontrib>Fu, Hui-Chuan</creatorcontrib><creatorcontrib>Tsay, Huey-Jen</creatorcontrib><creatorcontrib>Huang, Tung-Fu</creatorcontrib><creatorcontrib>Chen, Yau-Hung</creatorcontrib><creatorcontrib>Hung, Shih-Chieh</creatorcontrib><title>Twist controls skeletal development and dorsoventral patterning by regulating runx2 in zebrafish</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Twist1a and twist1b are the principal components of twists that negatively regulate a number of cellular signaling events. Expression of runx2 and downstream targets is essential for skeletal development and ventral organizer formation and specification in early vertebrate embryos, but what controls ventral activity of maternal runx2 and how twists function in zebrafish embryogenesis still remain unclear.
By studying the loss of twist induced by injection of morpholino-oligonucleotide in zebrafish, we found that twist1a and twist1b, but not twist2 or twist3, were required for proper skeletal development and dorsoventral patterning in early embryos. Overexpression of twist1a or twist1b following mRNA injection resulted in deteriorated skeletal development and formation of typical dorsalized embryos, whereas knockdown of twist1a and twist1b led to the formation of abnormal embryos with enhanced skeletal formation and typical ventralized patterning. Overexpression of twist1a or twist1b decreased the expression of runx2b, whereas twist1a and twist1b knockdown increased runx2b expression. We have further demonstrated that phenotypes induced by twist1a and twist1b knockdown were rescued by runx2b knockdown.
Together, these results suggest that twist1a and twist1b control skeletal development and dorsoventral patterning by regulating runx2b in zebrafish and provide potential targets for the treatment of diseases or syndromes associated with decreased skeletal development.</description><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - physiology</subject><subject>Biology</subject><subject>Body Patterning - genetics</subject><subject>Bone Development - genetics</subject><subject>Cancer</subject><subject>Cbfa-1 protein</subject><subject>Clinical medicine</subject><subject>Danio rerio</subject><subject>Drosophila</subject><subject>Education</subject><subject>Embryogenesis</subject><subject>Embryonic development</subject><subject>Embryonic Development - genetics</subject><subject>Embryonic growth stage</subject><subject>Embryos</subject><subject>Epidemiology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Genomes</subject><subject>Hospitals</subject><subject>Hypoxia</subject><subject>Injection</subject><subject>Insects</subject><subject>Mammals</subject><subject>Medical research</subject><subject>Medical treatment</subject><subject>Mineralization</subject><subject>mRNA</subject><subject>Neurosciences</subject><subject>Oligonucleotides</subject><subject>Pattern formation</subject><subject>Proteins</subject><subject>RNA</subject><subject>Signaling</subject><subject>Studies</subject><subject>Therapeutics</subject><subject>Transcription factors</subject><subject>Transcription Factors - deficiency</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><subject>Zebrafish</subject><subject>Zebrafish - embryology</subject><subject>Zebrafish - genetics</subject><subject>Zebrafish Proteins - deficiency</subject><subject>Zebrafish Proteins - genetics</subject><subject>Zebrafish Proteins - physiology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYqPwDxBEQgJx0eKP2IlvkKaJj0qTJsHg1jjJSeri2p3tjI1fj0uzqUG7IFaU2H7Oa_v1OVn2HKMFpiV-t3aDt8osts7CAiFSUlI8yI6xoGTOCaIPD_6PsichrBFitOL8cXZECKpKIvBx9uPilw4xb5yN3pmQh59gICqTt3AFxm03YGOubJu3zgd3lXo-TW5VjOCttn1e3-Qe-sGouOv5wV6TXNv8N9RedTqsnmaPOmUCPBu_s-zbxw8Xp5_nZ-eflqcnZ_OGCxznNUeiEUzx3aPK9NaqQ1XDSkYJdIxiVvNCcSoYr6qyKOuOs4o2nWCAm4LQWfZyr7s1LsjRnCAxxYgzQRlKxHJPtE6t5dbrjfI30ikt_w4430vlo24MyEIpACVAFQUqWEEVCCRIhau6AtximrTej6sN9QbaZu_LRHQ6Y_VK9u5KUoIRTvuZZW9GAe8uBwhRbnRowBhlwQ1BCsR4idNFJ_LVP-T9hxupXqX9a9u5tGyz05QnRckrTmmya5Yt7qFSa2GjUw5Ap9P4JODtJGCXJ3AdezWEIJdfv_w_e_59yr4-YFegTFwFZ4aonQ1TsNiDjXcheOjuPMZI7urg1g25qwM51kEKe3F4P3dBt4lP_wCHYgMp</recordid><startdate>20111107</startdate><enddate>20111107</enddate><creator>Yang, Der-Chih</creator><creator>Tsai, Chih-Chien</creator><creator>Liao, Yun-Feng</creator><creator>Fu, Hui-Chuan</creator><creator>Tsay, Huey-Jen</creator><creator>Huang, Tung-Fu</creator><creator>Chen, Yau-Hung</creator><creator>Hung, Shih-Chieh</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20111107</creationdate><title>Twist controls skeletal development and dorsoventral patterning by regulating runx2 in zebrafish</title><author>Yang, Der-Chih ; Tsai, Chih-Chien ; Liao, Yun-Feng ; Fu, Hui-Chuan ; Tsay, Huey-Jen ; Huang, Tung-Fu ; Chen, Yau-Hung ; Hung, Shih-Chieh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-b609c95a66666a766abaf08c57532ef5315b64a6395688747bf6583cf95e1c423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - physiology</topic><topic>Biology</topic><topic>Body Patterning - genetics</topic><topic>Bone Development - genetics</topic><topic>Cancer</topic><topic>Cbfa-1 protein</topic><topic>Clinical medicine</topic><topic>Danio rerio</topic><topic>Drosophila</topic><topic>Education</topic><topic>Embryogenesis</topic><topic>Embryonic development</topic><topic>Embryonic Development - genetics</topic><topic>Embryonic growth stage</topic><topic>Embryos</topic><topic>Epidemiology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Genomes</topic><topic>Hospitals</topic><topic>Hypoxia</topic><topic>Injection</topic><topic>Insects</topic><topic>Mammals</topic><topic>Medical research</topic><topic>Medical treatment</topic><topic>Mineralization</topic><topic>mRNA</topic><topic>Neurosciences</topic><topic>Oligonucleotides</topic><topic>Pattern formation</topic><topic>Proteins</topic><topic>RNA</topic><topic>Signaling</topic><topic>Studies</topic><topic>Therapeutics</topic><topic>Transcription factors</topic><topic>Transcription Factors - deficiency</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - physiology</topic><topic>Zebrafish</topic><topic>Zebrafish - embryology</topic><topic>Zebrafish - genetics</topic><topic>Zebrafish Proteins - deficiency</topic><topic>Zebrafish Proteins - genetics</topic><topic>Zebrafish Proteins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Der-Chih</creatorcontrib><creatorcontrib>Tsai, Chih-Chien</creatorcontrib><creatorcontrib>Liao, Yun-Feng</creatorcontrib><creatorcontrib>Fu, Hui-Chuan</creatorcontrib><creatorcontrib>Tsay, Huey-Jen</creatorcontrib><creatorcontrib>Huang, Tung-Fu</creatorcontrib><creatorcontrib>Chen, Yau-Hung</creatorcontrib><creatorcontrib>Hung, Shih-Chieh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Der-Chih</au><au>Tsai, Chih-Chien</au><au>Liao, Yun-Feng</au><au>Fu, Hui-Chuan</au><au>Tsay, Huey-Jen</au><au>Huang, Tung-Fu</au><au>Chen, Yau-Hung</au><au>Hung, Shih-Chieh</au><au>Milstone, David S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Twist controls skeletal development and dorsoventral patterning by regulating runx2 in zebrafish</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-11-07</date><risdate>2011</risdate><volume>6</volume><issue>11</issue><spage>e27324</spage><epage>e27324</epage><pages>e27324-e27324</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Twist1a and twist1b are the principal components of twists that negatively regulate a number of cellular signaling events. Expression of runx2 and downstream targets is essential for skeletal development and ventral organizer formation and specification in early vertebrate embryos, but what controls ventral activity of maternal runx2 and how twists function in zebrafish embryogenesis still remain unclear.
By studying the loss of twist induced by injection of morpholino-oligonucleotide in zebrafish, we found that twist1a and twist1b, but not twist2 or twist3, were required for proper skeletal development and dorsoventral patterning in early embryos. Overexpression of twist1a or twist1b following mRNA injection resulted in deteriorated skeletal development and formation of typical dorsalized embryos, whereas knockdown of twist1a and twist1b led to the formation of abnormal embryos with enhanced skeletal formation and typical ventralized patterning. Overexpression of twist1a or twist1b decreased the expression of runx2b, whereas twist1a and twist1b knockdown increased runx2b expression. We have further demonstrated that phenotypes induced by twist1a and twist1b knockdown were rescued by runx2b knockdown.
Together, these results suggest that twist1a and twist1b control skeletal development and dorsoventral patterning by regulating runx2b in zebrafish and provide potential targets for the treatment of diseases or syndromes associated with decreased skeletal development.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22087291</pmid><doi>10.1371/journal.pone.0027324</doi><tpages>e27324</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2011-11, Vol.6 (11), p.e27324-e27324 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1310659350 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Basic Helix-Loop-Helix Transcription Factors - physiology Biology Body Patterning - genetics Bone Development - genetics Cancer Cbfa-1 protein Clinical medicine Danio rerio Drosophila Education Embryogenesis Embryonic development Embryonic Development - genetics Embryonic growth stage Embryos Epidemiology Gene expression Gene Expression Regulation, Developmental Genomes Hospitals Hypoxia Injection Insects Mammals Medical research Medical treatment Mineralization mRNA Neurosciences Oligonucleotides Pattern formation Proteins RNA Signaling Studies Therapeutics Transcription factors Transcription Factors - deficiency Transcription Factors - genetics Transcription Factors - physiology Zebrafish Zebrafish - embryology Zebrafish - genetics Zebrafish Proteins - deficiency Zebrafish Proteins - genetics Zebrafish Proteins - physiology |
| title | Twist controls skeletal development and dorsoventral patterning by regulating runx2 in zebrafish |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T23%3A05%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Twist%20controls%20skeletal%20development%20and%20dorsoventral%20patterning%20by%20regulating%20runx2%20in%20zebrafish&rft.jtitle=PloS%20one&rft.au=Yang,%20Der-Chih&rft.date=2011-11-07&rft.volume=6&rft.issue=11&rft.spage=e27324&rft.epage=e27324&rft.pages=e27324-e27324&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0027324&rft_dat=%3Cgale_plos_%3EA476863358%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1310659350&rft_id=info:pmid/22087291&rft_galeid=A476863358&rft_doaj_id=oai_doaj_org_article_4aaeea9ea4404543ae9092818b8e1d13&rfr_iscdi=true |