Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells
Identifieur interne : 000A91 ( Main/Exploration ); précédent : 000A90; suivant : 000A92Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells
Auteurs : Lindsay Marek [États-Unis] ; Valerie Levresse [États-Unis] ; Claudia Amura [États-Unis] ; Eve Zentrich [États-Unis] ; Vicki Van Putten [États-Unis] ; Raphael A. Nemenoff [États-Unis] ; Lynn E. Heasley [États-Unis]Source :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2004-12.
English descriptors
- Teeft :
- Activator, Affymetrix, Biol, Biol chem, Cell differentiation, Cell extracts, Chem, Collaborative, Collaborative action, Collapsin response mediator protein, Conduit, Cortexin, Differentiation program, Erks, Extracellular, Extracellular kinase, Gene, Gene expression, Genechip, Global gene expression, Growth factor, Growth factors, Horse serum, Human synapsin, Independent experiments, Induction, Inhibitor, Kinase, Light chain, Mapk, Mapk pathways, Mapks, Marek, Mrna, Multiple signal conduits, Muscle cells, Nerve growth factor, Neural differentiation, Neuronal, Neuronal differentiation, Nflc, Nflc promoter, Pathway, Pheochromocytoma cells, Plasminogen, Previous study, Primer, Proc natl acad, Promoter, Protein kinase, Receptor, Signal conduit, Signal conduits, Synapsin, Synapsin reporter, Tgfb1, Transcription, Transcriptional, Transcriptional regulation, Transfected, Transfected cells, Upar, Urokinase plasminogen activator receptor, Zentrich.
Abstract
PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jcp.20087
Affiliations:
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Physiol.</title><idno type="ISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-12">2004-12</date><biblScope unit="volume">201</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="459">459</biblScope><biblScope unit="page" to="469">469</biblScope></imprint><idno type="ISSN">0021-9541</idno></series><idno type="istex">02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000</idno><idno type="DOI">10.1002/jcp.20087</idno><idno type="ArticleID">JCP20087</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Activator</term><term>Affymetrix</term><term>Biol</term><term>Biol chem</term><term>Cell differentiation</term><term>Cell extracts</term><term>Chem</term><term>Collaborative</term><term>Collaborative action</term><term>Collapsin response mediator protein</term><term>Conduit</term><term>Cortexin</term><term>Differentiation program</term><term>Erks</term><term>Extracellular</term><term>Extracellular kinase</term><term>Gene</term><term>Gene expression</term><term>Genechip</term><term>Global gene expression</term><term>Growth factor</term><term>Growth factors</term><term>Horse serum</term><term>Human synapsin</term><term>Independent experiments</term><term>Induction</term><term>Inhibitor</term><term>Kinase</term><term>Light chain</term><term>Mapk</term><term>Mapk pathways</term><term>Mapks</term><term>Marek</term><term>Mrna</term><term>Multiple signal conduits</term><term>Muscle cells</term><term>Nerve growth factor</term><term>Neural differentiation</term><term>Neuronal</term><term>Neuronal differentiation</term><term>Nflc</term><term>Nflc promoter</term><term>Pathway</term><term>Pheochromocytoma cells</term><term>Plasminogen</term><term>Previous study</term><term>Primer</term><term>Proc natl acad</term><term>Promoter</term><term>Protein kinase</term><term>Receptor</term><term>Signal conduit</term><term>Signal conduits</term><term>Synapsin</term><term>Synapsin reporter</term><term>Tgfb1</term><term>Transcription</term><term>Transcriptional</term><term>Transcriptional regulation</term><term>Transfected</term><term>Transfected cells</term><term>Upar</term><term>Urokinase plasminogen activator receptor</term><term>Zentrich</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li></region></list><tree><country name="États-Unis"><region name="Colorado"><name sortKey="Marek, Lindsay" sort="Marek, Lindsay" uniqKey="Marek L" first="Lindsay" last="Marek">Lindsay Marek</name></region><name sortKey="Amura, Claudia" sort="Amura, Claudia" uniqKey="Amura C" first="Claudia" last="Amura">Claudia Amura</name><name sortKey="Heasley, Lynn E" sort="Heasley, Lynn E" uniqKey="Heasley L" first="Lynn E." last="Heasley">Lynn E. Heasley</name><name sortKey="Heasley, Lynn E" sort="Heasley, Lynn E" uniqKey="Heasley L" first="Lynn E." last="Heasley">Lynn E. Heasley</name><name sortKey="Levresse, Valerie" sort="Levresse, Valerie" uniqKey="Levresse V" first="Valerie" last="Levresse">Valerie Levresse</name><name sortKey="Nemenoff, Raphael A" sort="Nemenoff, Raphael A" uniqKey="Nemenoff R" first="Raphael A." last="Nemenoff">Raphael A. Nemenoff</name><name sortKey="Putten, Vicki Van" sort="Putten, Vicki Van" uniqKey="Putten V" first="Vicki Van" last="Putten">Vicki Van Putten</name><name sortKey="Zentrich, Eve" sort="Zentrich, Eve" uniqKey="Zentrich E" first="Eve" last="Zentrich">Eve Zentrich</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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