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H3K36 methylation

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https://www.readbyqxmd.com/read/29027902/independent-manipulation-of-histone-h3-modifications-in-individual-nucleosomes-reveals-the-contributions-of-sister-histones-to-transcription
#1
Zhen Zhou, Yu-Ting Liu, Li Ma, Ting Gong, Yanan Hu, Hong-Tao Li, Chen Cai, Ling-Li Zhang, Gang Wei, Jin-Qiu Zhou
Histone tail modifications can greatly influence chromatin-associated processes. Asymmetrically modified nucleosomes exist in multiple cell types; however, whether modifications on both sister histones contribute equally to chromatin dynamics remains elusive. Here, we devised a bivalent nucleosome system that allowed for the constitutive assembly of asymmetrically modified sister histone H3s in nucleosomes in Saccharomyces cerevisiae. The sister H3K36 methylations independently affected cryptic transcription in gene coding regions, whereas sister H3K79 methylation had cooperative effects on gene silencing near telomeres...
October 13, 2017: ELife
https://www.readbyqxmd.com/read/29018328/intermittent-ethanol-during-adolescence-leads-to-lasting-behavioral-changes-in-adulthood-and-alters-gene-expression-and-histone-methylation-in-the-pfc
#2
Jennifer T Wolstenholme, Tariq Mahmood, Guy M Harris, Shahroze Abbas, Michael F Miles
Adolescents primarily consume alcohol in binges, which can be particularly harmful to the developing frontal cortex and increase risk for an adult alcohol use disorder. We conducted a study investigating immediate and long lasting changes to the prefrontal cortex (PFC) transcriptome to determine the molecular mechanisms underlying adult ethanol behavioral sensitivity following binge ethanol in adolescence. DBA/2J mice were orally dosed with 4 g/kg ethanol intermittently from day 29 to 42. Adolescent mice were tested for anxiety-like behavior and ethanol sensitivity using the loss of righting reflex task...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28975546/histone-3-lysine-36-to-methionine-mutations-stably-interact-with-and-sequester-sdg8-in-arabidopsis-thaliana
#3
Guang Lin, Ying Zhou, Min Li, Yuda Fang
Post-transcriptional modifications of histones play important roles in various biological processes. Here, we report that Arabidopsis plants overexpressing histone H3 lysine to methionine mutations at histone H3.1K36 (H3.1K36M) and H3.3K36 (H3.3K36M) have serious developmental defects with early-flowering and change in the modifications of endogenous histone H3, including acetylation at lysine 9 (H3K9ac), trimethylation at lysine 27 (H3K27me3), di- and tri-methylation at lysine 36 (H3K36me2 and H3K36me3). In addition, H3K36M mutation alters its subcellular localization and interacts with H3K36 methyltransferase SDG8...
September 26, 2017: Science China. Life Sciences
https://www.readbyqxmd.com/read/28933651/characterization-of-h3-3k36m-as-a-tool-to-study-h3k36-methylation-in-cancer-cells
#4
Saumya M Sankaran, Or Gozani
Recurrent mutations at key lysine residues in the histone variant H3.3 are thought to play an etiologic role in the development of distinct subsets of pediatric gliomas and bone and cartilage cancers. H3.3K36M is one such mutation that was originally identified in chondroblastomas, and its expression in these tumors contributes to oncogenic reprogramming by triggering global depletion of dimethylation and trimethylation at H3K36 with a concomitant increase in the levels of H3K27 trimethylation. H3.3K36M expression can also cause epigenomic changes in cell types beyond chondrocytic cells...
September 21, 2017: Epigenetics: Official Journal of the DNA Methylation Society
https://www.readbyqxmd.com/read/28903048/set2-methyltransferase-facilitates-dna-replication-and-promotes-genotoxic-stress-responses-through-mbf-dependent-transcription
#5
Chen-Chun Pai, Anastasiya Kishkevich, Rachel S Deegan, Andrea Keszthelyi, Lisa Folkes, Stephen E Kearsey, Nagore De León, Ignacio Soriano, Robertus Antonius Maria de Bruin, Antony M Carr, Timothy C Humphrey
Chromatin modification through histone H3 lysine 36 methylation by the SETD2 tumor suppressor plays a key role in maintaining genome stability. Here, we describe a role for Set2-dependent H3K36 methylation in facilitating DNA replication and the transcriptional responses to both replication stress and DNA damage through promoting MluI cell-cycle box (MCB) binding factor (MBF)-complex-dependent transcription in fission yeast. Set2 loss leads to reduced MBF-dependent ribonucleotide reductase (RNR) expression, reduced deoxyribonucleoside triphosphate (dNTP) synthesis, altered replication origin firing, and a checkpoint-dependent S-phase delay...
September 12, 2017: Cell Reports
https://www.readbyqxmd.com/read/28895528/a-synthetic-biology-approach-to-probing-nucleosome-symmetry
#6
Yuichi Ichikawa, Caitlin F Connelly, Alon Appleboim, Thomas Cr Miller, Hadas Jacobi, Nebiyu A Abshiru, Hsin-Jung Chou, Yuanyuan Chen, Upasna Sharma, Yupeng Zheng, Paul M Thomas, Hsuiyi V Chen, Vineeta Bajaj, Christoph W Müller, Neil L Kelleher, Nir Friedman, Daniel Na Bolon, Oliver J Rando, Paul D Kaufman
The repeating subunit of chromatin, the nucleosome, includes two copies of each of the four core histones, and several recent studies have reported that asymmetrically-modified nucleosomes occur at regulatory elements in vivo. To probe the mechanisms by which histone modifications are read out, we designed an obligate pair of H3 heterodimers, termed H3X and H3Y, which we extensively validated genetically and biochemically. Comparing the effects of asymmetric histone tail point mutants with those of symmetric double mutants revealed that a single methylated H3K36 per nucleosome was sufficient to silence cryptic transcription in vivo...
September 12, 2017: ELife
https://www.readbyqxmd.com/read/28852847/distinct-molecular-profile-of-diffuse-cerebellar-gliomas
#7
Masashi Nomura, Akitake Mukasa, Genta Nagae, Shogo Yamamoto, Kenji Tatsuno, Hiroki Ueda, Shiro Fukuda, Takayoshi Umeda, Tomonari Suzuki, Ryohei Otani, Keiichi Kobayashi, Takashi Maruyama, Shota Tanaka, Shunsaku Takayanagi, Takahide Nejo, Satoshi Takahashi, Koichi Ichimura, Taishi Nakamura, Yoshihiro Muragaki, Yoshitaka Narita, Motoo Nagane, Keisuke Ueki, Ryo Nishikawa, Junji Shibahara, Hiroyuki Aburatani, Nobuhito Saito
Recent studies have demonstrated that tumor-driving alterations are often different among gliomas that originated from different brain regions and have underscored the importance of analyzing molecular characteristics of gliomas stratified by brain region. Therefore, to elucidate molecular characteristics of diffuse cerebellar gliomas (DCGs), 27 adult, mostly glioblastoma cases were analyzed. Comprehensive analysis using whole-exome sequencing, RNA sequencing, and Infinium methylation array (n = 17) demonstrated their distinct molecular profile compared to gliomas in other brain regions...
August 29, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28790329/kdm4b-mediated-reduction-of-h3k9me3-and-h3k36me3-levels-improves-somatic-cell-reprogramming-into-pluripotency
#8
Jingwei Wei, Jisha Antony, Fanli Meng, Paul MacLean, Rebekah Rhind, Götz Laible, Björn Oback
Correct reprogramming of epigenetic marks is essential for somatic cells to regain pluripotency. Repressive histone (H) lysine (K) methylation marks are known to be stable and difficult to reprogram. In this study, we generated transgenic mice and mouse embryonic fibroblasts (MEFs) for the inducible expression of KDM4B, a demethylase that removes H3 K9 and H3K36 trimethylation (me3) marks (H3K9/36me3). Upon inducing Kdm4b, H3K9/36me3 levels significantly decreased compared to non-induced controls. Concurrently, H3K9me1 levels significantly increased, while H3K9me2 and H3K27me3 remained unchanged...
August 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28754676/nsd1-inactivation-and-setd2-mutation-drive-a-convergence-toward-loss-of-function-of-h3k36-writers-in-clear-cell-renal-cell-carcinomas
#9
Xiaoping Su, Jianping Zhang, Roger Mouawad, Eva Compérat, Morgan Roupret, Frederick Allanic, Jérôme Parra, Marc-Olivier Bitker, Erika J Thompson, Banumathy Gowrishankar, Jane Houldsworth, John N Weinstein, Jörg Tost, Bradley M Broom, David Khayat, Jean-Philippe Spano, Nizar M Tannir, Gabriel G Malouf
Extensive dysregulation of chromatin-modifying genes in clear-cell renal cell carcinoma (ccRCC) has been uncovered through next-generation sequencing. However, a scientific understanding of the crosstalk between epigenetic and genomic aberrations remains limited. Here we identify three ccRCC epigenetic clusters, including a clear-cell CpG island methylator phenotype (C-CIMP) subgroup associated with promoter methylation of vascular endothelial growth factor receptor genes (FLT4, FLT1 and KDR). C-CIMP was furthermore characterized by silencing of genes related to vasculature development...
July 28, 2017: Cancer Research
https://www.readbyqxmd.com/read/28753426/methyltransferase-setd2-mediated-methylation-of-stat1-is-critical-for-interferon-antiviral-activity
#10
Kun Chen, Juan Liu, Shuxun Liu, Meng Xia, Xiaomin Zhang, Dan Han, Yingming Jiang, Chunmei Wang, Xuetao Cao
Interferon-α (IFNα) signaling is essential for antiviral response via induction of IFN-stimulated genes (ISGs). Through a non-biased high-throughput RNAi screening of 711 known epigenetic modifiers in cellular models of IFNα-mediated inhibition of HBV replication, we identified methyltransferase SETD2 as a critical amplifier of IFNα-mediated antiviral immunity. Conditional knockout mice with hepatocyte-specific deletion of Setd2 exhibit enhanced HBV infection. Mechanistically, SETD2 directly mediates STAT1 methylation on lysine 525 via its methyltransferase activity, which reinforces IFN-activated STAT1 phosphorylation and antiviral cellular response...
July 27, 2017: Cell
https://www.readbyqxmd.com/read/28718400/histone-h3g34r-mutation-causes-replication-stress-homologous-recombination-defects-and-genomic-instability-in-s-pombe
#11
Rajesh K Yadav, Carolyn M Jablonowski, Alfonso G Fernandez, Brandon R Lowe, Ryan A Henry, David Finkelstein, Kevin J Barnum, Alison L Pidoux, Yin-Ming Kuo, Jie Huang, Matthew J O'Connell, Andrew J Andrews, Arzu Onar-Thomas, Robin C Allshire, Janet F Partridge
Recurrent somatic mutations of H3F3A in aggressive pediatric high-grade gliomas generate K27M or G34R/V mutant histone H3.3. H3.3-G34R/V mutants are common in tumors with mutations in p53 and ATRX, an H3.3-specific chromatin remodeler. To gain insight into the role of H3-G34R, we generated fission yeast that express only the mutant histone H3. H3-G34R specifically reduces H3K36 tri-methylation and H3K36 acetylation, and mutants show partial transcriptional overlap with set2 deletions. H3-G34R mutants exhibit genomic instability and increased replication stress, including slowed replication fork restart, although DNA replication checkpoints are functional...
July 18, 2017: ELife
https://www.readbyqxmd.com/read/28715960/histone-methylation-by-set-domain-proteins-in-fungi
#12
Michael Freitag
Histone-modifying enzymes are responsible for regulating transcription, recombination, DNA repair, DNA replication, chromatid cohesion, and chromosome segregation. Fungi are ideally suited for comparative chromatin biology because sequencing of numerous genomes from many clades is coupled to existing rich methodology that allows truly holistic approaches, integrating evolutionary biology with mechanistic molecular biology and ecology, promising applications in medicine or plant pathology. While genome information is rich, mechanistic studies on histone modifications are largely restricted to two yeasts, Saccharomyces cerevisiae and Schizosaccharomyces pombe, and one filamentous fungus, Neurospora crassa-three species that arguably are not representative of this diverse kingdom...
July 17, 2017: Annual Review of Microbiology
https://www.readbyqxmd.com/read/28663576/setd2-and-histone-h3-lysine-36-methylation-deficiency-in-advanced-systemic-mastocytosis
#13
G Martinelli, M Mancini, C De Benedittis, M Rondoni, C Papayannidis, M Manfrini, M Meggendorfer, R Calogero, V Guadagnuolo, M C Fontana, L Bavaro, A Padella, E Zago, L Pagano, R Zanotti, L Scaffidi, G Specchia, F Albano, S Merante, C Elena, P Savini, D Gangemi, P Tosi, F Ciceri, G Poletti, L Riccioni, F Morigi, M Delledonne, T Haferlach, M Cavo, P Valent, S Soverini
The molecular basis of advanced systemic mastocytosis (SM) is not fully understood and despite novel therapies the prognosis remains dismal. Exome sequencing of an index-patient with mast cell leukemia (MCL) uncovered biallelic loss-of-function mutations in the SETD2 histone methyltransferase gene. Copy-neutral loss-of-heterozygosity at 3p21.3 (where SETD2 maps) was subsequently found in SM patients and prompted us to undertake an in-depth analysis of SETD2 copy number, mutation status, transcript expression and methylation levels, as well as functional studies in the HMC-1 cell line and in a validation cohort of 57 additional cases with SM, including MCL, aggressive SM and indolent SM...
June 16, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28654864/wolf-hirschhorn-syndrome-candidate-1-whsc1-functions-as-a-tumor-suppressor-by-governing-cell-differentiation
#14
Chuan Yu, Xiaomin Yao, Linjie Zhao, Ping Wang, Qian Zhang, Chengjian Zhao, Shaohua Yao, Yuquan Wei
Wolf-Hirschhorn syndrome candidate 1 (WHSC1) is a histone 3 lysine 36 (H3K36) specific methyltransferase that is frequently deleted in Wolf-Hirschhorn syndrome (WHS). Whsc1 is also found mutated in a subgroup of B-cell derived malignant diseases by genomic translocation or point mutation, both of which resulted in hyperactivity of WHSC1 mediated H3K36 methylation and uncontrolled cell proliferation, suggesting that whsc1 functions as an oncogene. However, here we provided evidences to show that whsc1 also has tumor suppressor functions...
June 24, 2017: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/28614721/h3k36-methylation-regulates-nutrient-stress-response-in-saccharomyces-cerevisiae-by-enforcing-transcriptional-fidelity
#15
Stephen L McDaniel, Austin J Hepperla, Jie Huang, Raghuvar Dronamraju, Alexander T Adams, Vidyadhar G Kulkarni, Ian J Davis, Brian D Strahl
Set2-mediated histone methylation at H3K36 regulates diverse activities, including DNA repair, mRNA splicing, and suppression of inappropriate (cryptic) transcription. Although failure of Set2 to suppress cryptic transcription has been linked to decreased lifespan, the extent to which cryptic transcription influences other cellular functions is poorly understood. Here, we uncover a role for H3K36 methylation in the regulation of the nutrient stress response pathway. We found that the transcriptional response to nutrient stress was dysregulated in SET2-deleted (set2Δ) cells and was correlated with genome-wide bi-directional cryptic transcription that originated from within gene bodies...
June 13, 2017: Cell Reports
https://www.readbyqxmd.com/read/28601046/lsd1-knockdown-reveals-novel-histone-lysine-methylation-in-human-breast-cancer-mcf-7-cells
#16
Yue Jin, Bo Huo, Xueqi Fu, Zhongyi Cheng, Jun Zhu, Yu Zhang, Tian Hao, Xin Hu
Histone lysine methylation, which plays an important role in the regulation of gene expression, genome stability, chromosome conformation and cell differentiation, is a dynamic process that is collaboratively regulated by lysine methyltransferases (KMTs) and lysine demethylases (KDMs). LSD1, the first identified KDMs, catalyzes the demethylation of mono- and di-methylated H3K4 and H3K9. Here, we systematically investigated the effects of LSD1 knockdown on histone methylations. Surprisingly, in addition to H3K4 and H3K9, the methylation level on other histone lysines, such as H3K27, H3K36 and H3K79, are also increased...
August 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28498454/identification-of-setd2-nf1-fusion-gene-in-a-pediatric-spindle-cell-tumor-with-the-chromosomal-translocation-t-3-17-p21-q12
#17
Ioannis Panagopoulos, Ludmila Gorunova, Ingvild Lobmaier, Bodil Bjerkehagen, Sverre Heim
Spindle cell tumors are clinically heterogeneous but morphologically similar neoplasms. The term refers to the tumor cells' long and slender microscopic appearance. Distinct subgroups of spindle cell tumors are characterized by chromosomal translocations and also fusion genes. Other spindle cell tumors exist that have not yet been found to have characteristic, let alone pathognomonic, genetic or pathogenetic features. Continuous examination of spindle cell tumors is likely to reveal other subgroups that may, in the future, be seen to correspond to meaningful clinical differences and may even be therapeutically decisive...
June 2017: Oncology Reports
https://www.readbyqxmd.com/read/28483910/rna-binding-by-histone-methyltransferases-set1-and-set2
#18
Camille Sayou, Gonzalo Millán-Zambrano, Helena Santos-Rosa, Elisabeth Petfalski, Samuel Robson, Jonathan Houseley, Tony Kouzarides, David Tollervey
Histone methylation at H3K4 and H3K36 is commonly associated with genes actively transcribed by RNA polymerase II (RNAPII) and is catalyzed by Saccharomyces cerevisiae Set1 and Set2, respectively. Here we report that both methyltransferases can be UV cross-linked to RNA in vivo High-throughput sequencing of the bound RNAs revealed strong Set1 enrichment near the transcription start site, whereas Set2 was distributed along pre-mRNAs. A subset of transcripts showed notably high enrichment for Set1 or Set2 binding relative to RNAPII, suggesting functional posttranscriptional interactions...
July 15, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28413449/links-between-dna-methylation-and-nucleosome-occupancy-in-the-human-genome
#19
Clayton K Collings, John N Anderson
BACKGROUND: DNA methylation is an epigenetic modification that is enriched in heterochromatin but depleted at active promoters and enhancers. However, the debate on whether or not DNA methylation is a reliable indicator of high nucleosome occupancy has not been settled. For example, the methylation levels of DNA flanking CTCF sites are higher in linker DNA than in nucleosomal DNA, while other studies have shown that the nucleosome core is the preferred site of methylation. In this study, we make progress toward understanding these conflicting phenomena by implementing a bioinformatics approach that combines MNase-seq and NOMe-seq data and by comprehensively profiling DNA methylation and nucleosome occupancy throughout the human genome...
2017: Epigenetics & Chromatin
https://www.readbyqxmd.com/read/28394464/novel-mca-id-syndrome-with-ash1l-mutation
#20
Nobuhiko Okamoto, Fuyuki Miya, Tatsuhiko Tsunoda, Mitsuhiro Kato, Shinji Saitoh, Mami Yamasaki, Yonehiro Kanemura, Kenjiro Kosaki
We identified a novel mutation in ASH1L in a patient with severe intellectual disability, growth failure, microcephaly, facial dysmorphism, myelination delay, and skeletal abnormalities. ASH1L is a histone methyltransferase that associates with the transcribed region of all active genes examined, including Hox genes. It catalyzes H3K36 methylation and plays important roles in development. There has been increasing evidence that heterozygous mutation of ASH1L is associated with ID and autism spectrum disorders...
June 2017: American Journal of Medical Genetics. Part A
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