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Epigenomes, Volume 1, Issue 1 (June 2017)

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Editorial

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Open AccessEditorial Welcome to the New Journal Epigenomes
Epigenomes 2017, 1(1), 1; doi:10.3390/epigenomes1010001
Received: 16 February 2016 / Accepted: 16 February 2016 / Published: 7 April 2016
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Abstract We are excited to introduce Epigenomes, a new journal that will serve the growing community of researchers who use omic approaches to dissect the epigenetic mechanisms underlying developmental and pathological processes.[...] Full article

Research

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Open AccessArticle Helicase Lymphoid-Specific Enzyme Contributes to the Maintenance of Methylation of SST1 Pericentromeric Repeats That Are Frequently Demethylated in Colon Cancer and Associate with Genomic Damage
Epigenomes 2017, 1(1), 2; doi:10.3390/epigenomes1010002
Received: 27 July 2016 / Revised: 8 September 2016 / Accepted: 14 September 2016 / Published: 22 September 2016
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Abstract
DNA hypomethylation at repetitive elements accounts for the genome-wide DNA hypomethylation common in cancer, including colorectal cancer (CRC). We identified a pericentromeric repeat element called SST1 frequently hypomethylated (>5% demethylation compared with matched normal tissue) in several cancers, including 28 of 128 (22%)
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DNA hypomethylation at repetitive elements accounts for the genome-wide DNA hypomethylation common in cancer, including colorectal cancer (CRC). We identified a pericentromeric repeat element called SST1 frequently hypomethylated (>5% demethylation compared with matched normal tissue) in several cancers, including 28 of 128 (22%) CRCs. SST1 somatic demethylation associated with genome damage, especially in tumors with wild-type TP53. Seven percent of the 128 CRCs exhibited a higher (“severe”) level of demethylation (≥10%) that co-occurred with TP53 mutations. SST1 demethylation correlated with distinct histone marks in CRC cell lines and primary tumors: demethylated SST1 associated with high levels of the repressive histone 3 lysine 27 trimethylation (H3K27me3) mark and lower levels of histone 3 lysine 9 trimethylation (H3K9me3). Furthermore, induced demethylation of SST1 by 5-aza-dC led to increased H3K27me3 and reduced H3K9me3. Thus, in some CRCs, SST1 demethylation reflects an epigenetic reprogramming associated with changes in chromatin structure that may affect chromosomal integrity. The chromatin remodeler factor, the helicase lymphoid-specific (HELLS) enzyme, called the “epigenetic guardian of repetitive elements”, interacted with SST1 as shown by chromatin immunoprecipitation, and down-regulation of HELLS by shRNA resulted in demethylation of SST1 in vitro. Altogether these results suggest that HELLS contributes to SST1 methylation maintenance. Alterations in HELLS recruitment and function could contribute to the somatic demethylation of SST1 repeat elements undergone before and/or during CRC pathogenesis. Full article
(This article belongs to the Special Issue Biological Methylation in Development and Cancer)
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Open AccessArticle The Pea (Pisum sativum L.) Rogue Paramutation is Accompanied by Alterations in the Methylation Pattern of Specific Genomic Sequences
Epigenomes 2017, 1(1), 6; doi:10.3390/epigenomes1010006
Received: 28 February 2017 / Revised: 5 May 2017 / Accepted: 11 May 2017 / Published: 18 May 2017
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Abstract
The spontaneous emergence among common pea (Pisum sativum L.) cultivars of off-type rogue plants exhibiting leaves with narrower and pointed leaflets and stipules and the non-Mendelian inheritance of this new phenotype were first described in the early 20th century. However, so far,
[...] Read more.
The spontaneous emergence among common pea (Pisum sativum L.) cultivars of off-type rogue plants exhibiting leaves with narrower and pointed leaflets and stipules and the non-Mendelian inheritance of this new phenotype were first described in the early 20th century. However, so far, no studies at the molecular level of this first identified case of paramutation have been carried out. In this study, we show for the first time that the pea rogue paramutation is accompanied by alterations in the methylation status of specific genomic sequences. Although, no significant differences were observed in the genome-wide DNA methylation in leaves of non-rogue cv. Onward in comparison to its rogue paramutant line JI2723, 22 DNA sequences were identified by methylation-sensitive amplified fragment length polymorphisms (MS-AFLP) analysis as differentially methylated in the two epigenomes. Mitotically inherited through all leaf tissues, the differential methylation patterns were also found to be meiotically inherited and conserved in pollen grains for 12 out of the 22 sequences. Fourteen of the sequences were successfully amplified in cDNA but none of them exhibited significant differential expression in the two contrasting epigenotypes. The further exploitation of the present research results on the way towards the elucidation of the molecular mechanisms behind this interesting epigenetic phenomenon is discussed. Full article
(This article belongs to the Special Issue Plant Epigenome Dynamics)
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Review

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Open AccessReview New Frontiers in Melanoma Epigenetics—The More We Know, the More We Don’t Know
Epigenomes 2017, 1(1), 3; doi:10.3390/epigenomes1010003
Received: 31 December 2016 / Accepted: 25 January 2017 / Published: 30 January 2017
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Abstract
Skin cancer is one of the most common neoplasms worldwide, with a surprising tendency to increase its incidence. As with many cancer types nowadays, early diagnosis and proper management carries an excellent prognosis, up to 5-year survival rate of above 95% for most
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Skin cancer is one of the most common neoplasms worldwide, with a surprising tendency to increase its incidence. As with many cancer types nowadays, early diagnosis and proper management carries an excellent prognosis, up to 5-year survival rate of above 95% for most skin cancers, even though the long-term survival rate among metastatic melanoma patients remains only 5%. This review aims to summarize recent discoveries in epigenetic changes connected with cutaneous malignant melanoma (CMM), comprising of DNA methylation, histone modifications, miRNA regulation, nucleosome positioning and chromatin remodelling. Undoubtedly, personalised medicine based on both genetic and epigenetic changes of cancer is the future, the question remains: how long will it take to transport this treatment from the bench to the bedside? Full article
(This article belongs to the Special Issue Biological Methylation in Development and Cancer)
Open AccessReview Lysine-Specific Histone Demethylases Contribute to Cellular Differentiation and Carcinogenesis
Epigenomes 2017, 1(1), 4; doi:10.3390/epigenomes1010004
Received: 9 February 2017 / Revised: 24 March 2017 / Accepted: 24 March 2017 / Published: 30 March 2017
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Abstract
Histone modifications regulate chromatin structure, gene transcription, and other nuclear processes. Among the histone modifications, methylation has been considered to be a stable, irreversible process due to the slow turnover of methyl groups in chromatin. However, the discovery of three different classes of
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Histone modifications regulate chromatin structure, gene transcription, and other nuclear processes. Among the histone modifications, methylation has been considered to be a stable, irreversible process due to the slow turnover of methyl groups in chromatin. However, the discovery of three different classes of lysine-specific demethylases—KDM1, Jumonji domain-containing demethylases, and lysyl oxidase-like 2 protein—has drastically changed this view, suggesting a role for dynamic histone methylation in different biological process. In this review, we describe the different mechanisms that these enzymes use to remove lysine histone methylation and discuss their role during physiological (cell differentiation) and pathological (carcinogenesis) processes. Full article
(This article belongs to the Special Issue Biological Methylation in Development and Cancer)
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Open AccessReview Driver or Passenger: Epigenomes in Alzheimer’s Disease
Epigenomes 2017, 1(1), 5; doi:10.3390/epigenomes1010005
Received: 17 March 2017 / Revised: 26 April 2017 / Accepted: 26 April 2017 / Published: 30 April 2017
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Abstract
Alzheimer’s disease (AD) is a fatal neurodegenerative disease which is on the rise worldwide. Despite a wealth of information, genetic factors contributing to the emergence of AD still remain incompletely understood. Sporadic AD is polygenetic in nature and is associated with various environmental
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Alzheimer’s disease (AD) is a fatal neurodegenerative disease which is on the rise worldwide. Despite a wealth of information, genetic factors contributing to the emergence of AD still remain incompletely understood. Sporadic AD is polygenetic in nature and is associated with various environmental risks. Epigenetic mechanisms are well-recognized in the mediation of gene environment interactions, and analysis of epigenetic changes at the genome scale can offer new insights into the relationship between brain epigenomes and AD. In fact, recent epigenome-wide association studies (EWAS) indicate that changes in DNA methylation are an early event preceding clinical manifestation and are tightly associated with AD neuropathology. Further, candidate genes from EWAS interact with those from genome-wide association studies (GWAS) that can undergo epigenetic changes in their upstream gene regulatory elements. Functionally, AD-associated DNA methylation changes partially influence transcription of candidate genes involved in pathways relevant to AD. The timing of epigenomic changes in AD together with the genes affected indicate a critical role, however, further mechanistic insight is required to corroborate this hypothesis. In this respect, recent advances in neuronal reprogramming of patient-derived cells combined with new genome-editing techniques offer unprecedented opportunities to dissect the functional and mechanistic role of epigenomic changes in AD. Full article
(This article belongs to the Special Issue Epigenetics of the Nervous System)
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