Calcium regulation of neuronal gene expression.
Anne E. West,Wen G. Chen,Matthew B. Dalva,Ricardo E. Dolmetsch,Jon M. Kornhauser,Adam J. Shaywitz,Mari A. Takasu,Xu Tao,Michael E. Greenberg +8 more
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TLDR
This work has characterized molecular mechanisms by which neuronal membrane depolarization and subsequent calcium influx into the cytoplasm lead to the induction of new gene transcription and refined and expand the working model of activity-induced gene induction in the brain.Abstract:Â
Plasticity is a remarkable feature of the brain, allowing neuronal structure and function to accommodate to patterns of electrical activity. One component of these long-term changes is the activity-driven induction of new gene expression, which is required for both the long-lasting long-term potentiation of synaptic transmission associated with learning and memory, and the activitydependent survival events that help to shape and wire the brain during development. We have characterized molecular mechanisms by which neuronal membrane depolarization and subsequent calcium influx into the cytoplasm lead to the induction of new gene transcription. We have identified three points within this cascade of events where the specificity of genes induced by different types of stimuli can be regulated. By using the induction of the gene that encodes brain-derived neurotrophic factor (BDNF) as a model, we have found that the ability of a calcium influx to induce transcription of this gene is regulated by the route of calcium entry into the cell, by the pattern of phosphorylation induced on the transcription factor cAMP-response element (CRE) binding protein (CREB), and by the complement of active transcription factors recruited to the BDNF promoter. These results refine and expand the working model of activity-induced gene induction in the brain, and help to explain how different types of neuronal stimuli can activate distinct transcriptional responses.read more
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Calcium signalling: dynamics, homeostasis and remodelling
TL;DR: The Ca2+-signalling toolkit is used to assemble signalling systems with very different spatial and temporal dynamics and has a direct role in controlling the expression patterns of its signalling systems that are constantly being remodelled in both health and disease.
Journal ArticleDOI
Function and Regulation of CREB Family Transcription Factors in the Nervous System
Bonnie E. Lonze,David D. Ginty +1 more
TL;DR: This review focuses on the current level of understanding of where, when, and how CREB family members function in the nervous system.
Journal ArticleDOI
HDAC2 negatively regulates memory formation and synaptic plasticity
Ji-Song Guan,Stephen J. Haggarty,Emanuela Giacometti,Jan Hermen Dannenberg,Jan Hermen Dannenberg,Nadine F. Joseph,Nadine F. Joseph,Jun Gao,Thomas J.F. Nieland,Ying Zhou,X. L. Wang,Ralph Mazitschek,James E. Bradner,Ronald A. DePinho,Rudolf Jaenisch,Li-Huei Tsai,Li-Huei Tsai +16 more
TL;DR: It is suggested that HDAC2 functions in modulating synaptic plasticity and long-lasting changes of neural circuits, which in turn negatively regulates learning and memory.
Journal ArticleDOI
DNA methylation-related chromatin remodeling in activity-dependent BDNF gene regulation.
TL;DR: It is reported that increased synthesis of brain-derived neurotrophic factor in neurons after depolarization correlates with a decrease in CpG methylation within the regulatory region of the Bdnf gene, suggesting that DNA methylation–related chromatin remodeling is important for activity-dependent gene regulation that may be critical for neural plasticity.
Journal ArticleDOI
Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2.
Wen G. Chen,Qiang Chang,Yingxi Lin,Alexander Meissner,Anne E. West,Eric C. Griffith,Rudolf Jaenisch,Michael E. Greenberg +7 more
TL;DR: It is found that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene and suggests that the deregulation of this process may underlie the pathology of RT T.
References
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TL;DR: This work was supported by a grant from the European Commission BIOMED2 (BMH4-CT96-0656) and has been endorsed by the Food and Drug Administration (FDA) for use in clinical practice.
Journal ArticleDOI
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