dunnettreader + article + epigenetics   9

Simon M. G. Braun and Sebastian Jessberger - Adult neurogenesis: mechanisms and functional significance (2014) | Development - online Journal of development biology
DEVELOPMENT AT A GLANCE -- Abstract - New neurons are generated throughout life in distinct regions of the mammalian brain. This process, called adult neurogenesis, has been implicated in physiological brain function, and failing or altered neurogenesis has been associated with a number of neuropsychiatric diseases. Here, we provide an overview of the mechanisms governing the neurogenic process in the adult brain and describe how new neurons may contribute to brain function in health and disease.
article  neuroscience  brain-development  brain  genetics  epigenetics  physiology  psychology  plasticity  neurogenesis  primates  molecular_biology  downloaded  EF-add 
november 2014 by dunnettreader
Jens Rister, Claude Desplan, and Daniel Vasiliauskas - Primer Series: Establishing and maintaining gene expression patterns: insights from sensory receptor patterning (2013)
Development. Feb 1, 2013; 140(3): 493–503. - doi: 10.1242/dev.079095 - PMCID: PMC3561783 - Primer Series - In this Primer, we summarize our current understanding of the mechanisms governing SR patterning in the fly retina, one of the best-understood systems for SR gene choice. We then compare these regulatory mechanisms with those used in the mouse retina and in the fly and mouse olfactory systems. -- Abstract - In visual and olfactory sensory systems with high discriminatory power, each sensory neuron typically expresses one, or very few, sensory receptor genes, excluding all others. Recent studies have provided insights into the mechanisms that generate and maintain sensory receptor expression patterns. Here, we review how this is achieved in the fly retina and compare it with the mechanisms controlling sensory receptor expression patterns in the mouse retina and in the mouse and fly olfactory systems. -- Introduction - Multicellular organisms are able to perceive and discriminate a broad range of environmental stimuli within a number of sensory modalities. To achieve this, the visual and olfactory systems deploy large numbers of sensory receptors (SRs). For example, five Rhodopsin genes are differentially expressed in the fly retina while over 1200 olfactory receptor genes are expressed in the nose of the mouse . In sensory systems of high discriminatory power, each sensory neuron generally expresses only one or very few SR gene(s), excluding all others . Importantly, the choice of expressing a particular SR determines the identity and response spectrum of the sensory neuron. Thus, each sensory neuron faces two regulatory challenges during its terminal differentiation: it first has to make an unambiguous choice of SR expression, and it must then maintain this decision throughout its lifespan. Failure in either case would compromise the ability of the sensory system to discriminate between stimuli. -- downloaded pdf to Note Keywords: Hippo pathway, Cell identity maintenance, Olfactory receptor, Opsin, Photoreceptor, Sensory --
article  neuroscience  brain  perception  sensation  brain-development  vision  molecular_biology  genetics  epigenetics  downloaded  EF-add 
november 2014 by dunnettreader
Kevin T. Eade, et al - Developmental Transcriptional Networks Are Required to Maintain Neuronal Subtype Identity in the Mature Nervous System (2012)
PLoS Genet. Feb 2012; 8(2): e1002501.-- doi: 10.1371/journal.pgen.1002501
PMCID: PMC3285578 -- Kevin T. Eade, Hailey A. Fancher, Marc S. Ridyard, and Douglas W. Allan* - William A. Harris, Editor -- Abstract - During neurogenesis, transcription factors combinatorially specify neuronal fates and then differentiate subtype identities by inducing subtype-specific gene expression profiles. But how is neuronal subtype identity maintained in mature neurons? Modeling this question in two Drosophila neuronal subtypes (Tv1 and Tv4), we test whether the subtype transcription factor networks that direct differentiation during development are required persistently for long-term maintenance of subtype identity. By conditional transcription factor knockdown in adult Tv neurons after normal development, we find that most transcription factors within the Tv1/Tv4 subtype transcription networks are indeed required to maintain Tv1/Tv4 subtype-specific gene expression in adults. Thus, gene expression profiles are not simply “locked-in,” but must be actively maintained by persistent developmental transcription factor networks. We also examined the cross-regulatory relationships between all transcription factors that persisted in adult Tv1/Tv4 neurons. We show that certain critical cross-regulatory relationships that had existed between these transcription factors during development were no longer present in the mature adult neuron. This points to key differences between developmental and maintenance transcriptional regulatory networks in individual neurons. Together, our results provide novel insight showing that the maintenance of subtype identity is an active process underpinned by persistently active, combinatorially-acting, developmental transcription factors. These findings have implications for understanding the maintenance of all long-lived cell types and the functional degeneration of neurons in the aging brain. -- downloaded pdf to Note
article  neuroscience  brain-development  brain-aging  genetics  epigenetics  molecular_biology  plasticity  downloaded  EF-add 
november 2014 by dunnettreader
Verena Wolfram and Richard A. Baines - Blurring the boundaries: developmental and activity-dependent determinants of neural circuits (2013
Trends in Neuroscience. Oct 2013; 36(10): 610–619. - doi: 10.1016/j.tins.2013.06.006
PMCID: PMC3794160 -- Abstract - The human brain comprises approximately 100 billion neurons that express a diverse, and often subtype-specific, set of neurotransmitters and voltage-gated ion channels. Given this enormous complexity, a fundamental question is how is this achieved? The acquisition of neurotransmitter phenotype was viewed as being set by developmental programs ‘hard wired’ into the genome. By contrast, the expression of neuron-specific ion channels was considered to be highly dynamic (i.e., ‘soft wired’) and shaped largely by activity-dependent mechanisms. Recent evidence blurs this distinction by showing that neurotransmitter phenotype can be altered by activity and that neuron type-specific ion channel expression can be set, and perhaps limited by, developmental programs. Better understanding of these early regulatory mechanisms may offer new avenues to avert the behavioral changes that are characteristic of many mental illnesses. -- downloaded pdf to Note
article  neuroscience  neuro-endocrine_system  brain  plasticity  psychology  genetics  epigenetics  downloaded  EF-add 
november 2014 by dunnettreader
Francisco J. Novo - Habit acquisition in the context of neuronal genomic and epigenomic mosaicism (2014)
Frontiers of Human Neuroscience. 2014; 8: 255. - doi: 10.3389/fnhum.2014.00255
PMCID: PMC4007014 -- See the article "Epigenetic Priming of Memory Updating during Reconsolidation to Attenuate Remote Fear Memories" in Cell, volume 156 on page 261. -- A recent paper (Gräff et al., 2014) shows that remote fear memories in mice can be stably attenuated with the administration of histone de-acetylase (HDAC) inhibitors during reconsolidation. This achieved persistent attenuation of remote memories, even though it is well established that the brief period of hippocampal neuroplasticity induced by recent memory recall is absent for remote memories. Apparently, such epigenetic intervention primed the expression of neuroplasticity-related genes. This work comes shortly after the finding (McConnell et al., 2013) that individual neurons show an extraordinary degree of genomic mosaicism. Sequencing the genomes of single human frontal cortex neurons, these authors found that up to 41% of neurons contain at least one de novo copy-number variant (CNV) of at least one megabase in size. Segmental duplications have greatly expanded in African great apes (Marques-Bonet et al., 2009), and it is possible that increased retrotransposon activity during human neurogenesis also contributes to this striking diversity in CNV numbers in neuronal genomes (Singer et al., 2010). Taken together, both studies support the notion that genomic and epigenomic mosaicism allows for the introduction of heritable changes at the single-cell level that promote neuronal plasticity, and thus help to explain how human actions can modify neural circuits involved in memory and learning. -- downloaded pdf to Note
article  genetics  epigenetics  primates  human_nature  brain  neuroscience  memory  learning  plasticity  downloaded  EF-add 
november 2014 by dunnettreader
David L. Molfese - Advancing Neuroscience through Epigenetics: Molecular Mechanisms of Learning and Memory (2011)
Dev Neuropsychol. Oct 2011; 36(7): 810–827. - doi: 10.1080/87565641.2011.606395 PMCID: PMC3191880 - NIHMSID: NIHMS325838 -- Abstract - Humans share 96% of our 30,000 genes with Chimpanzees. The 1,200 genes that differ appear at first glance insufficient to describe what makes us human and them apes. However, we are now discovering that the mechanisms that regulate how genes are expressed tell a much richer story than our DNA alone. Sections of our DNA are constantly being turned on or off, marked for easy access, or secluded and hidden away, all in response to on-going cellular activity. In the brain, neurons encode information – in effect memories – at the cellular level. Yet while memories may last a lifetime, neurons are dynamic structures. Every protein in the synapse undergoes some form of turnover, some with half-lives of only hours. How can a memory persist beyond the lifetimes of its constitutive molecular building blocks? Epigenetics – changes in gene expression that do not alter the underlying DNA sequence – may be the answer. In this article, epigenetic mechanisms including DNA methylation and acetylation or methylation of the histone proteins that package DNA are described in the context of animal learning. Through the interaction of these modifications a “histone code” is emerging wherein individual memories leave unique memory traces at the molecular level with distinct time courses. A better understanding of these mechanisms has implications for treatment of memory disorders caused by normal aging or diseases including schizophrenia, Alzheimer’s, depression, and drug addiction. -- downloaded pdf to Note - Keywords: epigenetics, genes, memory, learning, histone, hippocampus, behavior
article  genetics  epigenetics  memory  learning  brain  neuroscience  molecular_biology  primates  psychology  human_nature  downloaded  EF-add 
november 2014 by dunnettreader
Victoria Menzies, et al - Epigenetic Alterations and an Increased Frequency of Micronuclei in Women with Fibromyalgia (2013)
Nursing Research and Practice. 2013; doi: 10.1155/2013/795784 -- PMCID: PMC3766610 -- Victoria Menzies, 1 ,* Debra E. Lyon, 1 , 2 Kellie J. Archer, 3 Qing Zhou, 3 Jenni Brumelle, 4 Kimberly H. Jones, 4 , 5 G. Gao, 3 Timothy P. York, 6 and Colleen Jackson-Cook -- Abstract - Fibromyalgia (FM), characterized by chronic widespread pain, fatigue, and cognitive/mood disturbances, leads to reduced workplace productivity and increased healthcare expenses. To determine if acquired epigenetic/genetic changes are associated with FM, we compared the frequency of spontaneously occurring micronuclei (MN) and genome-wide methylation patterns in women with FM (n = 10) to those seen in comparably aged healthy controls (n = 42 (MN); n = 8 (methylation)). The mean (sd) MN frequency of women with FM (51.4 (21.9)) was significantly higher than that of controls (15.8 (8.5)) (χ2 = 45.552; df = 1; P = 1.49 × 10−11). Significant differences (n = 69 sites) in methylation patterns were observed between cases and controls considering a 5% false discovery rate. The majority of differentially methylated (DM) sites (91%) were attributable to increased values in the women with FM. The DM sites included significant biological clusters involved in neuron differentiation/nervous system development, skeletal/organ system development, and chromatin compaction. Genes associated with DM sites whose function has particular relevance to FM included BDNF, NAT15, HDAC4, PRKCA, RTN1, and PRKG1. Results support the need for future research to further examine the potential role of epigenetic and acquired chromosomal alterations as a possible biological mechanism underlying FM. -- downloaded pdf to Note
article  health  genetics  epigenetics  neuroscience  downloaded 
november 2014 by dunnettreader
Herb Gintis - Gene–culture coevolution and the nature of human sociality | Royal Society | Phil Trans B 2011
Published 14 February 2011 doi: 10.1098/rstb.2010.0310 Phil. Trans. R. Soc. B 27 March 2011 vol. 366 no. 1566 878-888 -- downloaded pdf to Note Abstract --
Human characteristics are the product of gene–culture coevolution, which is an evolutionary dynamic involving the interaction of genes and culture over long time periods. Gene–culture coevolution is a special case of niche construction. Gene–culture coevolution is responsible for human other-regarding preferences, a taste for fairness, the capacity to empathize and salience of morality and character virtues.
article  genetics  biocultural_evolution  epigenetics  human_nature  moral_psychology  moral_sentiments  character  downloaded  EF-add 
january 2014 by dunnettreader

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