Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2007-10-1
pubmed:abstractText
The small ubiquitin-related modifier (SUMO) is a member of the ubiquitin-like protein family, and SUMO conjugation (SUMOylation) resembles ubiquitination. Despite many SUMOylation target proteins being reported, the role of this system in vertebrate development remains unclear. We inhibited the function of Xenopus SUMO-1 (XSUMO-1) using a morpholino antisense oligo against XSUMO-1 (XSUMO-1-MO) to clarify the role of SUMOylation. XSUMO-1-MO inhibited normal axis formation in embryos and elongation of activin-treated animal caps. The expression of several mesoderm markers was reduced by XSUMO-1-MO. We measured activin-like activity by using a reporter construct containing a multimer of activin-responsive elements from the Goosecoid promoter, [DE(6x)Luc]. This assay showed that XSUMO-1-MO directly inhibited activin/nodal signaling. Furthermore, XSUMO-1-MO inhibited ectopic axis formation induced by XSmad2, and XSmad2/4 mRNA could not rescue the axis elongation defect induced by XSUMO-1-MO. These results suggested that XSUMO-1 is required for normal axis elongation, at least partly mediating activin/nodal signaling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1058-8388
pubmed:author
pubmed:copyrightInfo
2007 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
236
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2757-66
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
XSUMO-1 is required for normal mesoderm induction and axis elongation during early Xenopus development.
pubmed:affiliation
Department of Life Sciences (Biology), Graduate School of Arts and Sciences, University of Tokyo, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't