Linked Life Data

15736129

Source:http://linkedlifedata.com/resource/pubmed/id/15736129

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-3-7
pubmed:abstractText
Mitogen-activated protein kinase (MAPK) signaling pathways play an important role in controlling embryonic proliferation and differentiation. It has been demonstrated that sequential lipophilic signal transduction mediators that participate in the MAPK pathway are null post-implantation lethal. It is not clear why the lethality of these null mutants arises after implantation and not before. One hypothesis is that the gene product of these post-implantation lethal null mutants are not present before implantation in normal embryos and do not have function until after implantation. To test this hypothesis, we selected a set of lipophilic genes mediating MAPK signal transduction pathways whose null mutants result in early peri-implantation or placental lethality. These included FRS2alpha, GAB1, GRB2, SOS1, Raf-B, and Raf1. Products of these selected genes were detected and their locations and functions indicated by indirect immunocytochemistry and Western blotting for proteins and RT-polymerase chain reaction (PCR) for mRNA transcription. We report here that all six signal mediators are detected at the protein level in preimplantation mouse embryo, placental trophoblasts, and in cultured trophoblast stem cells (TSC). Proteins are all detected in E3.5 embryos at a time when the first known mitogenic intercellular communication has been documented. mRNA transcripts of two post-implantation null mutant genes are expressed in mouse preimplantation embryos and unfertilized eggs. These mRNA transcripts were detected as maternal mRNA in unfertilized eggs that could delay the lethality of null mutants. All of the proteins were detected in the cytoplasm or in the cell membrane. This study of spatial and temporal expression revealed that all of these six null mutants post-implantation genes in MAPK pathway are expressed and, where tested, phosphorylated/activated proteins are detected in the blastocyst. Studies on RNA expression using RT-PCR suggest that maternal RNA could play an important role in delaying the presence of the lethal phenotype of null mutations.
pubmed:grant
pubmed:keyword
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1040-452X
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2005 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-11
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15736129-Adaptor Proteins, Signal Transducing, pubmed-meshheading:15736129-Animals, pubmed-meshheading:15736129-Antibody Specificity, pubmed-meshheading:15736129-Blastocyst, pubmed-meshheading:15736129-Blotting, Western, pubmed-meshheading:15736129-Cell Line, pubmed-meshheading:15736129-Embryo Implantation, pubmed-meshheading:15736129-Fertilization, pubmed-meshheading:15736129-GRB2 Adaptor Protein, pubmed-meshheading:15736129-Gene Expression Regulation, Developmental, pubmed-meshheading:15736129-Genes, Lethal, pubmed-meshheading:15736129-Humans, pubmed-meshheading:15736129-Lipid Metabolism, pubmed-meshheading:15736129-MAP Kinase Signaling System, pubmed-meshheading:15736129-Membrane Proteins, pubmed-meshheading:15736129-Mice, pubmed-meshheading:15736129-Mice, Knockout, pubmed-meshheading:15736129-Ovum, pubmed-meshheading:15736129-RNA, Messenger, pubmed-meshheading:15736129-Stem Cells, pubmed-meshheading:15736129-Trophoblasts
pubmed:year
2005
pubmed:articleTitle
Six post-implantation lethal knockouts of genes for lipophilic MAPK pathway proteins are expressed in preimplantation mouse embryos and trophoblast stem cells.
pubmed:affiliation
CS Mott Center for Human Growth and Development of Ob/Gyn, Wayne State University School of Medicine, East Hancock, Detroit, Michigan 48201, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural