Linked Life Data

19517573

Source:http://linkedlifedata.com/resource/pubmed/id/19517573

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2009-6-24
pubmed:abstractText
The sea urchin oral-aboral (OA) axis is established in part by Nodal signaling. The OA axis is also influenced by treatments affecting respiration and Nodal transcription is influenced by redox-dependent transcription factors. This suggests that intracellular redox state plays a role in OA axis specification. Since cellular redox state can be altered by the formation of excess reactive oxygen species (ROS), and hypoxia and paraquat generate ROS in cells, we asked whether these treatments affected specification of the OA axis and Nodal expression. Embryos cultured under conditions that elevate ROS, demonstrate perturbed ectoderm specification, but other territories are not affected. Immunohistochemical and Q-RT-PCR analyses revealed that both oral and aboral ectoderm genes are downregulated. Our results argue that elevating ROS in sea urchin embryos by these treatments blocks early steps in ectoderm differentiation preceding the polarization of the ectoderm into oral and aboral territories.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1058-8388
pubmed:author
pubmed:copyrightInfo
(c) 2009 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
238
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1777-87
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Reduced O2 and elevated ROS in sea urchin embryos leads to defects in ectoderm differentiation.
pubmed:affiliation
Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't