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dc.contributor.authorJohnson, William Eustace Basil
dc.contributor.authorWai, Htoo Aung
dc.date.accessioned2020-06-24T10:00:21Z
dc.date.available2020-06-24T10:00:21Z
dc.date.issued2015-02-15
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/623512/Wai%20STEM%20CELLS%20AND%20DEVELOPMENT%202014.pdf?sequence=1
dc.identifier.citationWai, H. A., Kawakami, K., Wada, H., Müller, F., Vernallis, A. B., Brown, G., & Johnson, W. E. B. (2015). The development and growth of tissues derived from cranial neural crest and primitive mesoderm is dependent on the ligation status of retinoic acid receptor γ: evidence that retinoic acid receptor γ functions to maintain stem/progenitor cells in the absence of retinoic acid. Stem cells and development, 24(4), 507-519.en_US
dc.identifier.urihttp://hdl.handle.net/10034/623512
dc.descriptionAn important study demonstrating how retinoic acid receptor gamma plays a key role in tissue formation and regenerationen_US
dc.descriptionFinal publication is available from Mary Ann Liebert, Inc., publishers http://dx.doi.org/10.1089/scd.2014.0235
dc.description.abstractRetinoic acid (RA) signaling is important to normal development. However, the function of the different RA receptors (RARs)--RARα, RARβ, and RARγ--is as yet unclear. We have used wild-type and transgenic zebrafish to examine the role of RARγ. Treatment of zebrafish embryos with an RARγ-specific agonist reduced somite formation and axial length, which was associated with a loss of hoxb13a expression and less-clear alterations in hoxc11a or myoD expression. Treatment with the RARγ agonist also disrupted formation of tissues arising from cranial neural crest, including cranial bones and anterior neural ganglia. There was a loss of Sox 9-immunopositive neural crest stem/progenitor cells in the same anterior regions. Pectoral fin outgrowth was blocked by RARγ agonist treatment. However, there was no loss of Tbx-5-immunopositive lateral plate mesodermal stem/progenitor cells and the block was reversed by agonist washout or by cotreatment with an RARγ antagonist. Regeneration of the caudal fin was also blocked by RARγ agonist treatment, which was associated with a loss of canonical Wnt signaling. This regenerative response was restored by agonist washout or cotreatment with the RARγ antagonist. These findings suggest that RARγ plays an essential role in maintaining stem/progenitor cells during embryonic development and tissue regeneration when the receptor is in its nonligated state.en_US
dc.publisherMary Ann Liebert, Incen_US
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4313414/pdf/scd.2014.0235.pdfen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/en_US
dc.subjectStem cellsen_US
dc.subjectRetinoic aciden_US
dc.subjectTissue formation and regenerationen_US
dc.titleThe Development and Growth of Tissues Derived From Cranial Neural Crest and Primitive Mesoderm Is Dependent on the Ligation Status of Retinoic Acid Receptor γ: Evidence That Retinoic Acid Receptor γ Functions to Maintain stem/progenitor Cells in the Absence of Retinoic Aciden_US
dc.typeArticleen_US
dc.identifier.eissn1557-8534en_US
dc.contributor.departmentAston Universityen_US
dc.identifier.journalStem Cells and Developmenten_US
or.grant.openaccessYesen_US
rioxxterms.funderWe are grateful to the Charles Wallace Trust for their financial support of H.A.W. The research leading to these results has received funding from the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme FP7/2007–2013/under REA grant agreement number 315902. G.B. and W.E.B.J. are partners within the Marie Curie Initial Training Network DECIDE (decision-making within cells and differentiation entity therapies).en_US
rioxxterms.identifier.projectUnfundeden_US
rioxxterms.versionAMen_US
rioxxterms.versionofrecordhttps://doi.org/10.1089/scd.2014.0235en_US
rioxxterms.licenseref.startdate2016-02-15
refterms.dateFCD2020-06-23T14:49:03Z
refterms.versionFCDAM
refterms.dateFOA2020-06-24T10:00:22Z
rioxxterms.publicationdate2015-02-15
dc.dateAccepted2014-09-18
dc.date.deposited2020-06-24en_US
dc.indentifier.issn1547-3287en_US


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