Epigenetics & Chromatin

Description

  • Impact factor
    4.19
  • 5-year impact
    4.18
  • Cited half-life
    2.60
  • Immediacy index
    1.11
  • Eigenfactor
    0.00
  • Article influence
    2.24
  • Website
  • Other titles
    Epigenetics and chromatin
  • ISSN
    1756-8935
  • OCLC
    263688252
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

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    ABSTRACT: Epigenetic mechanisms create variably stable changes in gene expression through the establishment of heritable states of chromatin architecture. While many epigenetic phenomena are, by definition, heritably passed through cell division during animal and plant development, evidence suggests that 'epigenetic states' may also be inherited across multiple generations. Work in the nematode Caenorhabditis elegans has uncovered a number of mechanisms that participate in regulating the transgenerational passage of epigenetic states. These mechanisms include some that establish and maintain heritable epigenetic information in the form of histone modifications, as well as those that filter the epigenetic information that is stably transmitted. The information appears to influence and help guide or regulate gene activity and repression in subsequent generations. Genome surveillance mechanisms guided by small RNAs appear to be involved in identifying and directing heritable repression of genomic elements, and thus may participate in filtering information that is inappropriate for stable transmission. This review will attempt to summarize recent findings that illustrate this simple nematode to be a truly elegant resource for defining emerging biological paradigms.As the cell lineage that links generations, the germline is the carrier of both genetic and epigenetic information. Like genetic information, information in the epigenome can heritably affect gene regulation and phenotype; yet unlike genetic information, the epigenome of the germ lineage is highly modified within each generation. Despite such alterations, some epigenetic information is highly stable across generations, leading to transgenerationally stable phenotypes that are unlinked to genetic changes. Studies in the nematode C. elegans have uncovered mechanisms that contribute to transgenerational repression as well as to the expression of genes that rely on histone modifying machinery and/or non-coding RNA-based mechanisms. These studies indicate that epigenetic mechanisms operating within the germ cell cycle of this organism filter and maintain an epigenetic memory that is required for germ cell function and can also influence gene expression in somatic lineages.
    Epigenetics & Chromatin 03/2014; 7(1):6.
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    ABSTRACT: X chromosome inactivation (XCI) is a developmental program of heterochromatin formation that initiates during early female mammalian embryonic development and is maintained through a lifetime of cell divisions in somatic cells. Despite identification of the crucial long non-coding RNA Xist and involvement of specific chromatin modifiers in the establishment and maintenance of the heterochromatin of the inactive X chromosome (Xi), interference with known pathways only partially reactivates the Xi once silencing has been established. Here, we studied ATF7IP (MCAF1), a protein previously characterized to coordinate DNA methylation and histone H3K9 methylation through interactions with the methyl-DNA binding protein MBD1 and the histone H3K9 methyltransferase SETDB1, as a candidate maintenance factor of the Xi.
    Epigenetics & Chromatin 01/2014; 7:12.
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    ABSTRACT: Targeted gene silencing is an important approach in both drug development and basic research. However, the selection of a potent suppressor has become a significant hurdle to implementing maximal gene inhibition for this approach. We attempted to construct a 'super suppressor' by combining the activities of two suppressors that function through distinct epigenetic mechanisms.
    Epigenetics & Chromatin 01/2014; 7:20.
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    ABSTRACT: Differential distribution of DNA methylation on the parental alleles of imprinted genes distinguishes the alleles from each other and dictates their parent of origin-specific expression patterns. While differential DNA methylation at primary imprinting control regions is inherited via the gametes, additional allele-specific DNA methylation is acquired at secondary sites during embryonic development and plays a role in the maintenance of genomic imprinting. The precise mechanisms by which this somatic DNA methylation is established at secondary sites are not well defined and may vary as methylation acquisition at these sites occurs at different times for genes in different imprinting clusters.
    Epigenetics & Chromatin 01/2014; 7:9.
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    ABSTRACT: Within the nucleus of eukaryotic cells, chromatin is organized into compact, silent regions called heterochromatin and more loosely packaged regions of euchromatin where transcription is more active. Although the existence of heterochromatin has been known for many years, the cellular factors responsible for its formation have only recently been identified. Two key factors involved in heterochromatin formation in Drosophila are the H3 lysine 9 methyltransferase Su(var)3-9 and heterochromatin protein 1 (HP1). The linker histone H1 also plays a major role in heterochromatin formation in Drosophila by interacting with Su(var)3-9 and helping to recruit it to heterochromatin. Drosophila STAT (Signal transducer and activator of transcription) (STAT92E) has also been shown to be involved in the maintenance of heterochromatin, but its relationship to the H1-Su(var)3-9 heterochromatin pathway is unknown. STAT92E is also involved in tumor formation in flies. Hyperactive Janus kinase (JAK)-STAT signaling due to a mutation in Drosophila JAK (Hopscotch) causes hematopoietic tumors.
    Epigenetics & Chromatin 01/2014; 7:16.
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    ABSTRACT: Dendritic cells (DCs) are important mediators of innate and adaptive immune responses, but the gene networks governing their lineage differentiation and maturation are poorly understood. To gain insight into the mechanisms that promote human DC differentiation and contribute to the acquisition of their functional phenotypes, we performed genome-wide base-resolution mapping of 5-methylcytosine in purified monocytes and in monocyte-derived immature and mature DCs.
    Epigenetics & Chromatin 01/2014; 7:21.
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    ABSTRACT: Cellular differentiation and reprogramming are accompanied by changes in replication timing and 3D organization of large-scale (400 to 800 Kb) chromosomal domains ('replication domains'), but few gene products have been identified whose disruption affects these properties. Here we show that deletion of esBAF chromatin-remodeling complex components BAF250a and Brg1, but not BAF53a, disrupts replication timing at specific replication domains. Also, BAF250a-deficient fibroblasts reprogrammed to a pluripotency-like state failed to reprogram replication timing in many of these same domains. About half of the replication domains affected by Brg1 loss were also affected by BAF250a loss, but a much larger set of domains was affected by BAF250a loss. esBAF binding in the affected replication domains was dependent upon BAF250a but, most affected domains did not contain genes whose transcription was affected by loss of esBAF. Loss of specific esBAF complex subunits alters replication timing of select replication domains in pluripotent cells.
    Epigenetics & Chromatin 12/2013; 6(1):42.

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