File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Eya1 interacts with Six2 and Myc to regulate expansion of the nephron progenitor pool during nephrogenesis

TitleEya1 interacts with Six2 and Myc to regulate expansion of the nephron progenitor pool during nephrogenesis
Authors
Issue Date2014
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/devcel
Citation
Developmental Cell, 2014, v. 31 n. 4, p. 434-447 How to Cite?
AbstractSelf-renewal and proliferation of nephron progenitor cells and the decision to initiate nephrogenesis are crucial events directing kidney development. Despite recent advancements in defining lineage and regulators for the progenitors, fundamental questions about mechanisms driving expansion of the progenitors remain unanswered. Here we show that Eya1 interacts with Six2 and Myc to control self-renewing cell activity. Cell fate tracing reveals a developmental restriction of the Eya1(+) population within the intermediate mesoderm to nephron-forming cell fates and a common origin shared between caudal mesonephric and metanephric nephrons. Conditional inactivation of Eya1 leads to loss of Six2 expression and premature epithelialization of the progenitors. Six2 mediates translocation of Eya1 to the nucleus, where Eya1 uses its threonine phosphatase activity to control Myc phosphorylation/dephosphorylation and function in the progenitor cells. Our results reveal a functional link between Eya1, Six2, and Myc in driving the expansion and maintenance of the multipotent progenitors during nephrogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/207985
ISSN
2015 Impact Factor: 9.338
2015 SCImago Journal Rankings: 7.338
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, J-
dc.contributor.authorWong, YME-
dc.contributor.authorCheng, C-
dc.contributor.authorLi, J-
dc.contributor.authorSharkar, MTK-
dc.contributor.authorXu, CY-
dc.contributor.authorChen, B-
dc.contributor.authorSun, J-
dc.contributor.authorJing, D-
dc.contributor.authorXu, PX-
dc.date.accessioned2015-02-02T04:27:38Z-
dc.date.available2015-02-02T04:27:38Z-
dc.date.issued2014-
dc.identifier.citationDevelopmental Cell, 2014, v. 31 n. 4, p. 434-447-
dc.identifier.issn1534-5807-
dc.identifier.urihttp://hdl.handle.net/10722/207985-
dc.description.abstractSelf-renewal and proliferation of nephron progenitor cells and the decision to initiate nephrogenesis are crucial events directing kidney development. Despite recent advancements in defining lineage and regulators for the progenitors, fundamental questions about mechanisms driving expansion of the progenitors remain unanswered. Here we show that Eya1 interacts with Six2 and Myc to control self-renewing cell activity. Cell fate tracing reveals a developmental restriction of the Eya1(+) population within the intermediate mesoderm to nephron-forming cell fates and a common origin shared between caudal mesonephric and metanephric nephrons. Conditional inactivation of Eya1 leads to loss of Six2 expression and premature epithelialization of the progenitors. Six2 mediates translocation of Eya1 to the nucleus, where Eya1 uses its threonine phosphatase activity to control Myc phosphorylation/dephosphorylation and function in the progenitor cells. Our results reveal a functional link between Eya1, Six2, and Myc in driving the expansion and maintenance of the multipotent progenitors during nephrogenesis.-
dc.languageeng-
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/devcel-
dc.relation.ispartofDevelopmental Cell-
dc.titleEya1 interacts with Six2 and Myc to regulate expansion of the nephron progenitor pool during nephrogenesisen_US
dc.typeArticleen_US
dc.identifier.emailWong, YME: elainewg@hku.hk-
dc.identifier.doi10.1016/j.devcel.2014.10.015-
dc.identifier.pmid25458011-
dc.identifier.pmcidPMC4282136-
dc.identifier.scopuseid_2-s2.0-84921318905-
dc.identifier.hkuros267225-
dc.identifier.volume31-
dc.identifier.issue4-
dc.identifier.spage434-
dc.identifier.epage447-
dc.identifier.isiWOS:000345540200009-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats