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Regulation of gene transcription by neuronal activity is evident in a large number of neuronal processes ranging from neural development and refinement of neuronal connections to learning and response to injury. In the field of activity-dependent gene expression, rapid progress is being made that can impact these, and many other areas of neuroscience. This book offers an up-to-date picture of the field.
This book discusses the regulation of gene transcription by neuronal activity that is evident in a large number of neuronal processes ranging from neural development and refinement of neuronal connections to learning and response to injury. Transcriptional Regulation by Neuronal Activity: To the Nucleus and Back, 2nd edition illustrates how signals are transmitted to the nucleus in response to neuronal activity, which genes are regulated and how this is achieved, and how these changes in gene expression alter neuronal function. The aim of this second edition is to highlight key advances in the field since the first edition. The book is divided into four sections. The first highlights how signals get to the nucleus from the membrane in response to synaptic or neuronal activity. Included are chapters on the pathways that transmit signals from synapses to nuclei. The second section focuses on epigenetic regulatory processes of activity-induced gene transcription, an area that has exploded in the past few years. The third section navigates the role of activity-induced genes in physiological processes such as learning and memory, and human developmental disorders such as those associated with the autism spectrum. The fourth section highlights groundbreaking technological advances in the field, which have allowed activity-regulated transcription to be used as a tool to study learning and memory.
The ability of extrinsic environmental cues to modify the nervous system is critical both for the appropriate maturation of the nervous system, as well as for important adaptive functions of the mature brain, such as learning and memory. The discovery that, in response to sensory experience, neurotransmitter release at synapses and subsequent calcium influx into postsynaptic neurons lead to the synthesis of new gene products suggested a compelling mechanism by which long-lasting, use-dependent changes occur in the nervous system. Despite considerable progress in our understanding of the program of neuronal activity-regulated gene expression, direct evidence that the activity-dependent component of transcription per se is specifically important for nervous system development or function has been elusive. The first part of this thesis addresses this question through the development of a mutant mouse model in which the activity-dependent component of Bdnf expression is specifically disrupted. We find that mutation of the CaRE3/CRE (CREm) at endogenous Bdnf promoter IV by gene targeting results in an animal in which the neuronal activity-dependent component of Bdnf transcription in the cortex is selectively disrupted. CREm knock-in mice exhibit a reduction in the number of inhibitory synapses formed by cortical neurons in culture, a reduction in spontaneous inhibitory quantal transmission measured in acute brain slices, and a reduction in the level of inhibitory presynaptic markers in the cortex.
The neural crest is a remarkable embryonic population of cells found only in vertebrates and has the potential to give rise to many different cell types contributing throughout the body. These derivatives range from the mesenchymal bone and cartilage comprising the facial skeleton, to neuronal derivatives of the peripheral sensory and autonomic nervous systems, to melanocytes throughout the body, and to smooth muscle of the great arteries of the heart. For these cells to correctly progress from an unspecifi ed, nonmigratory population to a wide array of dynamic, differentiated cell types-some of which retain stem cell characteristics presumably to replenish these derivatives-requires a complex network of molecular switches to control the gene programs giving these cells their defi ning structural, enzymatic, migratory, and signaling capacities. This review will bring together current knowledge of neural crest-specifi c transcription factors governing these progressions throughout the course of development. A more thorough understanding of the mechanisms of transcriptional control in differentiation will aid in strategies designed to push undifferentiated cells toward a particular lineage, and unraveling these processes will help toward reprogramming cells from a differentiated to a more naive state. Table of Contents: Introduction / AP Genes / bHLH Genes / ETS Genes / Fox Genes / Homeobox Genes / Hox Genes / Lim Genes / Pax Genes / POU Domain Genes / RAR/RXR Genes / Smad Genes / Sox Genes / Zinc Finger Genes / Other Miscellaneous Genes / References / Author Biographies
Long term memory is mediated by long-lasting forms of synaptic plasticity that require new gene transcription for their persistence. Previous work has shown that neuronal CREB-regulated transcriptional coactivator 1 (CRTC1) plays a crucial role during learning and memory by regulating activity-dependent gene expression. We have shown that CRTC1 undergoes synapse-to-nucleus translocation to regulate transcription of CREB target genes in response to neuronal activity. In this thesis, we investigate the regulation and retrograde transport of CRTC1 in neurons and examine the nuclear role of CRTC1 in activity-dependent gene transcription. Our first goal was to identify the mechanisms by which CRTC1 responds to activity. We describe key synaptic processes necessary to trigger dephosphorylation of three serine residues that are required for dynein-mediated transport of CRTC1 to the nucleus. Our second goal was to understand the role of CRCT1 as a transcriptional coactivator. We use a combination of ChIP-seq, ATAC-seq and RNA-seq to understand how CRTC1 binding to CREB and other transcription factors correlates with changes in chromatin accessibility and transcription of activity-induced genes. Finally, we summarize a series of projects that attempt to elucidate how regulation of CRTC1's phosphorylation code may influence its function in neurons. These studies highlight the complexities of CRTC1 as an intrinsically disordered protein with 50 phosphorylated residues and a variety of potential interacting partners.
Offers an up-to-date account of the latest research findings concerned with the regulatory mechanisms of gene expression in neuronal and glial cells under different conditions. The book explores the cellular and neurobiological aspects of important phenomena of the nervous system and its role in health, disease and injury. Contributions from prominent scientists in the field address a variety of specific topics concerned with gene expression in the nervous system--from growth, hormonal and trophic factors to neural tissue reactions in injury or aging.
Neuronal activity and subsequent calcium influx activates a signaling cascade that causes transcription factors in the nucleus to rapidly induce an early-response program of gene expression. This early-response program is composed of transcriptional regulators that in turn induce transcription of late-response genes, which are enriched for regulators of synaptic development and plasticity that act locally at the synapse.
This first book to cover neural development, neuronal survival and function on the genetic level outlines promising approaches for novel therapeutic strategies in fighting neurodegenerative disorders, such as Alzheimer's disease. Focusing on transcription factors, the text is clearly divided into three sections devoted to transcriptional control of neural development, brain function and transcriptional dysregulation induced neurological diseases. With a chapter written by Nobel laureate Eric Kandel, this is essential reading for neurobiologists, geneticists, biochemists, cell biologists, neurochemists and molecular biologists.
Mechanisms in Transcriptional Regulation provides a concisediscussion of the fundamental concepts in transcription and itsregulation. Covers RNA polymerases, transcriptional machinery, mechanismsof transcriptional activation, the histone code hypothesis, theepigenetic control of transcription, and combinatorial control insignaling and development Features over 80 figures available to download online Chapters include comprehensive reading lists, boxeshighlighting theoretical concepts and experimental methods andproblems designed to build and test understanding