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Epigenetic Processes (epigenetic + process)
Selected AbstractsAbscisic Acid-mediated Epigenetic Processes in Plant Development and Stress ResponsesJOURNAL OF INTEGRATIVE PLANT BIOLOGY, Issue 10 2008Viswanathan Chinnusamy Abstract Abscisic acid (ABA) regulates diverse plant processes, growth and development under non-stress conditions and plays a pivotal role in abiotic stress tolerance. Although ABA-regulated genetic processes are well known, recent discoveries reveal that epigenetic processes are an integral part of ABA-regulated processes. Epigenetic mechanisms, namely, histone modifications and cytosine DNA methylation-induced modification of genome give rise to epigenomes, which add diversity and complexity to the genome of organisms. Histone monoubiquitination appears to regulate ABA levels in developing seeds through histone H2B monoubiquitination. ABA and H2B ubiquitination dependent chromatin remodeling regulate seed dormancy. Transcription factor networks necessary for seed maturation are repressed by histone deacetylases (HDACs)-dependent and PICKLE chromatin remodeling complexes (CRCs), whereas ABA induces the expression of these genes directly or through repression of HDACs. Abiotic stress-induced ABA regulates stomatal response and stress-responsive gene expression through HDACs and HOS15-dependent histone deacetylation, as well as through the ATP-dependent SWITCH/SUCROSE NONFERMENTING CRC. ABA also probably regulates the abiotic stress response through DNA methylation and short interfering RNA pathways. Further studies on ABA-regulated epigenome will be of immense use to understand the plant development, stress adaptation and stress memory. [source] Epigenetic control of skeletal muscle fibre typeACTA PHYSIOLOGICA, Issue 4 2010K. Baar Abstract Adult muscle is extremely plastic. However, the muscle precursor cells associated with those fibres show stable and heritable differences in gene expression indicative of epigenetic imprinting. Epigenetic processes in the development of skeletal muscle have been appreciated for over a decade; however, there are a paucity of studies looking at whether epigenetics determines the phenotype of adult and/or ageing skeletal muscle. This review presents the evidence that epigenetics plays a role in determining adult muscle function and a series of unanswered questions that would greatly increase our understanding of how epigenetics works in adult muscle. With the increased interest in epigenetics, over the next few years this field will begin to unfold in unimaginable directions. [source] The Epigenesis of the Family System as a Context for Individual DevelopmentFAMILY PROCESS, Issue 3 2002Herta A. Guttman M.D. In this article, the concept introduced by Lyman Wynne, that the individual develops epigenetically within the family system, is discussed and validated with data from a study of the characteristics and relationships of 27 women with borderline personality disorder and their parents. Each stage of the epigenetic process is impaired in one way or another, adversely affecting subsequent stages. Early impairment of attachment-care-giving processes is at least partly attributable to a lack of empathic parenting; effective communication is marred by family members' inability to experience or express feelings (alexithymia); this, in turn, makes it difficult to engage in joint family problem solving. Mutuality between family members does not occur in such a context, and there is an absence of intimacy between family members. These are often abusive family systems, with multiple abuse and intrafamilial sexual abuse more specifically directed at the daughter with BPD. The symptoms of the daughter can be understood systemically, as representing both predispositional characteristics and reactions to the family system. It is suggested that the epigenetic paradigm could be used to characterize the specific failure of developmental processes in many different disorders. [source] Mechanisms of imprint dysregulation,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 3 2010Bernhard Horsthemke Abstract Genomic imprinting is an epigenetic process by which the male and the female germ line confer specific marks (imprints) onto certain gene regions, so that one allele of an imprinted gene is active and the other allele is silent. Genomic imprints are erased in primordial germ cells, newly established during later stages of germ cell development, and stably inherited through somatic cell divisions during postzygotic development. Defects in imprint erasure, establishment, or maintenance result in a paternal chromosome carrying a maternal imprint or in a maternal chromosome carrying a paternal imprint. A wrong imprint leads to activation of an allele that should be silent or silencing of an allele that should be active. Since the dosage of imprinted genes is very important for development and growth, imprinting defects lead to specific diseases. Imprinting defects can occur spontaneously without any DNA sequence change (primary imprinting defect) or as the result of a mutation in a cis -regulatory element or a trans -acting factor (secondary imprinting defect). The distinction between primary and secondary imprinting defects is important for assessing the recurrence risk in affected families. © 2010 Wiley-Liss, Inc. [source] Nonlinear epigenetic variance: review and simulationsDEVELOPMENTAL SCIENCE, Issue 1 2010Kees-Jan Kan We present a review of empirical evidence that suggests that a substantial portion of phenotypic variance is due to nonlinear (epigenetic) processes during ontogenesis. The role of such processes as a source of phenotypic variance in human behaviour genetic studies is not fully appreciated. In addition to our review, we present simulation studies of nonlinear epigenetic variance using a computational model of neuronal network development. In each simulation study, time series for monozygotic and dizygotic twins were generated and analysed using conventional behaviour genetic modelling. In the results of these analyses, the nonlinear epigenetic variance was subsumed under the non-shared environmental component. As is commonly found in behaviour genetic studies, observed heritabilities and unique environmentabilities increased with time, whereas common environmentabilities decreased. The fact that the phenotypic effects of nonlinear epigenetic processes appear as unsystematic variance in conventional twin analyses complicates the identification and quantification of the ultimate genetic and environmental causes of individual differences. We believe that nonlinear dynamical system theories provide a challenging perspective on the development of individual differences, which may enrich behaviour genetic studies. [source] oleed, a medaka Polycomb group gene, regulates ciliogenesis and left,right patterningGENES TO CELLS, Issue 12 2009Daisuke Arai Left-right (LR) patterning is an essential part of the animal body plan. Primary cilia are known to play a pivotal role in this process. In humans, genetic disorders of ciliogenesis cause serious congenital diseases. A comprehensive mechanism that regulates ciliogenesis has not been proposed so far. Here, we show that EED, a core member of the Polycomb group (PcG) genes and a presumed player in many epigenetic processes, is required for ciliogenesis and subsequent LR patterning in the medaka fish, Oryzias latipes. Moderate knockdown of oleed, a medaka homolog of EED, preferentially caused situs inversus. In the affected embryo, the cilia in Kupffer's vesicle showed various defects in their structure, position and motility. Furthermore, we demonstrated that oleed maintains the expression of Noto, which, in mice, regulates ciliogenesis and LR patterning. This study provides the first evidence for the involvement of epigenetic plasticity in LR patterning through ciliogenesis. [source] Abscisic Acid-mediated Epigenetic Processes in Plant Development and Stress ResponsesJOURNAL OF INTEGRATIVE PLANT BIOLOGY, Issue 10 2008Viswanathan Chinnusamy Abstract Abscisic acid (ABA) regulates diverse plant processes, growth and development under non-stress conditions and plays a pivotal role in abiotic stress tolerance. Although ABA-regulated genetic processes are well known, recent discoveries reveal that epigenetic processes are an integral part of ABA-regulated processes. Epigenetic mechanisms, namely, histone modifications and cytosine DNA methylation-induced modification of genome give rise to epigenomes, which add diversity and complexity to the genome of organisms. Histone monoubiquitination appears to regulate ABA levels in developing seeds through histone H2B monoubiquitination. ABA and H2B ubiquitination dependent chromatin remodeling regulate seed dormancy. Transcription factor networks necessary for seed maturation are repressed by histone deacetylases (HDACs)-dependent and PICKLE chromatin remodeling complexes (CRCs), whereas ABA induces the expression of these genes directly or through repression of HDACs. Abiotic stress-induced ABA regulates stomatal response and stress-responsive gene expression through HDACs and HOS15-dependent histone deacetylation, as well as through the ATP-dependent SWITCH/SUCROSE NONFERMENTING CRC. ABA also probably regulates the abiotic stress response through DNA methylation and short interfering RNA pathways. Further studies on ABA-regulated epigenome will be of immense use to understand the plant development, stress adaptation and stress memory. [source] Alterations in local chromatin environment are involved in silencing and activation of subtelomeric var genes in Plasmodium falciparumMOLECULAR MICROBIOLOGY, Issue 1 2007Till S. Voss Summary Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1), encoded by the var gene family, undergoes antigenic variation and plays an important role in chronic infection and severe malaria. Only a single var gene is transcribed per parasite, and epigenetic control mechanisms are fundamental in this strategy of mutually exclusive transcription. We show that subtelomeric upsB var gene promoters carried on episomes are silenced by default, and that promoter activation is sufficient to silence all other family members. However, they are active by default when placed downstream of a second active var promoter, underscoring the significance of local chromatin environment and nuclear compartmentalization in var promoter regulation. Native chromatin covering the SPE2 -repeat array in upsB promoters is resistant to nuclease digestion, and insertion of these regulatory elements into a heterologous promoter causes local alterations in nucleosomal organization and promoter repression. Our findings suggest a common logic underlying the transcriptional control of all var genes, and have important implications for our understanding of the epigenetic processes involved in the regulation of this major virulence gene family. [source] Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibilityTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 10 2008Jonathan Mill Attention-deficit hyperactivity disorder (ADHD) is a common childhood neurobehavioural disorder defined by symptoms of developmentally inappropriate inattention, impulsivity and hyperactivity. As is the norm for most psychiatric phenotypes, traditional aetiological studies have focused primarily on the interplay between genetic and environmental factors. It is likely that epigenetic factors, i.e., heritable, but reversible changes to genomic function that are independent of DNA sequence, are also important. It is known that epigenetic processes can be induced following exposure to a range of external factors, and thus provide a mechanism by which the environment can lead to long-term alterations in phenotype. In this article we hypothesise that epigenetic dysregulation may mediate the association observed between early-development environmental insults and ADHD. We propose that understanding the epigenetic processes involved in linking specific environmental pathogens to an increased risk for ADHD may offer new possibilities for preventative and therapeutic intervention. [source] |