The Signal Transduction Pathway Underlying Ion Channel Gene Regulation by Sp1-c-Jun Interactions
During neuronal differentiation, an exquisitely controlled program of signal transduction events takes place, leading to the temporally and spatially regulated expression of genes associated with the differentiated phenotype. A critical class of genes involved in this phenomenon is that made up of g...
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Published in | The Journal of biological chemistry Vol. 276; no. 22; pp. 19040 - 19045 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.06.2001
American Society for Biochemistry and Molecular Biology |
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Abstract | During neuronal differentiation, an exquisitely controlled program of signal transduction events takes place, leading to the temporally and spatially regulated expression of genes associated with the differentiated phenotype. A critical class of genes involved in this phenomenon is that made up of genes encoding neurotransmitter-gated ion channels that play a central role in signal generation and propagation within the nervous system. We used the well established PC12 cell line to investigate the molecular details underlying the expression of the neuronal nicotinic acetylcholine receptor class of ion channels. Neuronal differentiation of PC12 cells can be induced by nerve growth factor, leading to an increase in neuronal nicotinic acetylcholine receptor gene expression. Nerve growth factor initiates several signal transduction cascades. Here, we show that the Ras-dependent mitogen-activated protein kinase and phosphoinositide 3-kinase pathways are critical for the nerve growth factor-mediated increase in the transcriptional activity of a neuronal nicotinic acetylcholine receptor gene promoter. In addition, we show that a component of the Ras-dependent mitogen-activated protein kinase pathway, nerve growth factor-inducible c-Jun, exerts its effects on receptor gene promoter activity most likely through protein-protein interactions with Sp1. Finally, we demonstrate that the target for nerve growth factor signaling is an Sp1-binding site within the neuronal nicotinic acetylcholine receptor gene promoter. |
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AbstractList | During neuronal differentiation, an exquisitely controlled program of signal transduction events takes place, leading to the temporally and spatially regulated expression of genes associated with the differentiated phenotype. A critical class of genes involved in this phenomenon is that made up of genes encoding neurotransmitter-gated ion channels that play a central role in signal generation and propagation within the nervous system. We used the well established PC12 cell line to investigate the molecular details underlying the expression of the neuronal nicotinic acetylcholine receptor class of ion channels. Neuronal differentiation of PC12 cells can be induced by nerve growth factor, leading to an increase in neuronal nicotinic acetylcholine receptor gene expression. Nerve growth factor initiates several signal transduction cascades. Here, we show that the Ras-dependent mitogen-activated protein kinase and phosphoinositide 3- kinase pathways are critical for the nerve growth factor-mediated increase in the transcriptional activity of a neuronal nicotinic acetylcholine receptor gene promoter. In addition, we show that a component of the Ras-dependent mitogen-activated protein kinase pathway, nerve growth factor-inducible c-Jun, exerts its effects on receptor gene promoter activity most likely through protein-protein interactions with Sp1. Finally, we demonstrate that the target for nerve growth factor signaling is an Sp1-binding site within the neuronal nicotinic acetylcholine receptor gene promoter. During neuronal differentiation, an exquisitely controlled program of signal transduction events takes place, leading to the temporally and spatially regulated expression of genes associated with the differentiated phenotype. A critical class of genes involved in this phenomenon is that made up of genes encoding neurotransmitter-gated ion channels that play a central role in signal generation and propagation within the nervous system. We used the well established PC12 cell line to investigate the molecular details underlying the expression of the neuronal nicotinic acetylcholine receptor class of ion channels. Neuronal differentiation of PC12 cells can be induced by nerve growth factor, leading to an increase in neuronal nicotinic acetylcholine receptor gene expression. Nerve growth factor initiates several signal transduction cascades. Here, we show that the Ras-dependent mitogen-activated protein kinase and phosphoinositide 3-kinase pathways are critical for the nerve growth factor-mediated increase in the transcriptional activity of a neuronal nicotinic acetylcholine receptor gene promoter. In addition, we show that a component of the Ras-dependent mitogen-activated protein kinase pathway, nerve growth factor-inducible c-Jun, exerts its effects on receptor gene promoter activity most likely through protein-protein interactions with Sp1. Finally, we demonstrate that the target for nerve growth factor signaling is an Sp1-binding site within the neuronal nicotinic acetylcholine receptor gene promoter. |
Author | Melnikova, Irena N. Gardner, Paul D. |
Author_xml | – sequence: 1 givenname: Irena N. surname: Melnikova fullname: Melnikova, Irena N. – sequence: 2 givenname: Paul D. surname: Gardner fullname: Gardner, Paul D. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11262397$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Animals Binding Sites Blotting, Western c-Jun protein Cell Differentiation Cell Line Drosophila Ion Channels - metabolism MAP Kinase Signaling System Mutation Nerve Growth Factor - metabolism Nerve Growth Factor - pharmacology Neurons - cytology Neurons - metabolism PC12 Cells Phenotype Phosphatidylinositol 3-Kinases - metabolism Precipitin Tests Promoter Regions, Genetic Proto-Oncogene Proteins c-jun - metabolism Ras protein ras Proteins - metabolism Rats Receptors, Cholinergic - genetics Receptors, Cholinergic - metabolism Signal Transduction Sp1 Transcription Factor - metabolism Transcription, Genetic Transcriptional Activation Transfection |
Title | The Signal Transduction Pathway Underlying Ion Channel Gene Regulation by Sp1-c-Jun Interactions |
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