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Epigenetic Influences (epigenetic + influence)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

Epigenetic influence of social experiences across the lifespan

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 4 2010
Frances A. Champagne
Abstract The critical role of social interactions in driving phenotypic variation has long been inferred from the association between early social deprivation and adverse neurodevelopmental outcomes. Recent evidence has implicated molecular pathways involved in the regulation of gene expression as one possible route through which these long-term outcomes are achieved. These epigenetic effects, though not exclusive to social experiences, may be a mechanism through which the quality of the social environment becomes embedded at a biological level. Moreover, there is increasing evidence for the transgenerational impact of these early experiences mediated through changes in social and reproductive behavior exhibited in adulthood. In this review, recent studies which highlight the epigenetic effects of parent,offspring, peer and adult social interactions both with and across generations will be discussed and the implications of this research for understanding the developmental origins of individual differences in brain and behavior will be explored. © 2010 Wiley Periodicals, Inc. Dev Psychobiol 52: 299,311, 2010. [source]

Influence of metyrapone treatment during pregnancy on the development and maturation of brain monoaminergic systems in the rat

ACTA PHYSIOLOGICA, Issue 4 2009
M. L. Leret
Abstract Aim:, This study examines the effect of reducing the corticosterone levels of gestating rat dams on the postnatal development and maturation of monoaminergic systems in their offspring's brains. Methods:, Metyrapone, an inhibitor of CORT synthesis, was administered to pregnant rats from E0 to E17 of gestation. Monoamine concentrations were determined in male and female offspring at postnatal days (PN) 23 and 90 in the hippocampus, hypothalamus and striatum. Results:, Reducing maternal corticosterone (mCORT) during gestation led to alterations in dopamine and serotonin levels in all three brain areas studied at PN 23. Alterations persisted until at least PN 90 in the serotonergic systems; the dopamine content of the hippocampus also remained modified. Reduced mCORT during gestation also led to alterations in the development and maturation of the hypothalamic noradrenergic systems. Sexually dimorphic responses were observed in all these monoaminergic systems at different times. Conclusion:, These results suggest that while they are still developing, brain monoaminergic systems are particularly sensitive to epigenetic influences. An adequate foetal level of CORT is required for the normal ontogeny of brain monoaminergic systems. The present data also provide that during the critical period of brain development, maternal CORT plays an important role in the sexual differentiation of monoaminergic systems, with particular influence on brain serotonergic neurones. [source]

Rapid changes in clonal lines: the death of a ,sacred cow'

BIOLOGICAL JOURNAL OF THE LINNEAN SOCIETY, Issue 1 2003
HUGH D. LOXDALE
It is well established that asexually reproducing viruses and prokaryotes mutate rapidly. In contrast, the eukaryotic clone is often still treated as if it is genetically homogeneous within and between populations, i.e. that it is assumed to show genetic fidelity. However, such fidelity has rarely been tested empirically using the range of high-resolution molecular markers now available, culminating with direct sequencing of the DNA. If such a biological entity as a ,clone' really did exist, it would be a fantastic entity, differing from everything else known in biology, i.e. it would possess a population mean but no variance for any particular trait. It would not be amenable to selection and adaptive variation and would thus be unchanging in time and space. In this paper, we argue that the general acceptance of clonal fidelity is a scientific convenience, since the rate of asexual reproduction of eukaryotes is not as fast as that of bacteria and hence it is easier to accept fidelity as a ,fact' rather than test for it. We propose that part of the acceptance of fidelity may have a cultural basis and thereby is a kind of ,pre-Darwinian relic'. Instead, a clonal genotype is perhaps largely a function of marker resolution, i.e. dependent on the number and type of markers employed. If this is so and were enough of the genome explored, perhaps each individual within a clone would be found to differ genetically at particular regions of the chromosomes. The question of what constitutes a clone is not just a semantic one and impacts directly on recent attempts to understand and produce ,artificial' clones, especially of mammals. New research is already confirming that mutations and epigenetic influences play a crucial role in the success of cloning attempts. © 2003 The Linnean Society of London. Biological Journal of the Linnean Society, 2003, 79, 3,16. [source]

Novel and recurrent germline LEMD3 mutations causing Buschke,Ollendorff syndrome and osteopoikilosis but not isolated melorheostosis

CLINICAL GENETICS, Issue 6 2009
Y Zhang
Mutations in the LEMD3 gene were recently incriminated in Buschke,Ollendorff syndrome (BOS) and osteopoikilosis, with or without melorheostosis. The relationship of this gene with isolated sporadic melorheostosis is less clear. We investigated LEMD3 in a two-generation BOS family showing an extremely variable expression of the disease, in a sporadic patient with skin features of BOS, and in an additional subject with isolated melorheostosis. We identified two different mutations, both resulting in a premature stop codon, in the two cases of BOS. The mutation (c.2564G>A) reported in the familial case is novel, while that observed in the sporadic case (c.1963C>T) has been previously reported in an American woman with osteopoikilosis and melorheostosis who had a family history of isolated osteopoikilosis. The search for mutations in DNA extracted from the peripheral blood, as well as skin and bone biopsies of the patient with melorheostosis failed to identify any pathogenic change. Our results further expand the LEMD3 mutation repertoire, corroborate the extreme interfamilial and intrafamilial clinical variability of LEMD3 mutations, and underline the lack of a clear phenotype,genotype correlation in BOS. The present study supports the general conclusion that LEMD3 mutations do not contribute to isolated sporadic melorheostosis. The genetic or epigenetic influences that are responsible for the development of melorheostosis require further investigation. [source]