• Journal of Life Science
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• v.21 no.4
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• pp.616-620
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• 2011

Lysine residues of histone H3 and H4 are covalently modified in the chromatin of eukaryotic cells. Lysine 27 in histone H3 was acetylated (H3K27ac) or methylated at three levels; mono-, di-, and trimethylation (H3K27me1, H3K27me2, and H3K27me3). These modifications at H3K27 were related with gene transcription and/or chromatin structure in distinct patterns. Generally, H3K27ac and H3K27me1 were enriched in active chromatin, such as the locus control region or transcriptionally active genes, while transcriptionally inactive genes were highly marked by H3K27me2 and H3K27me3. These modifications appear to have been catalyzed by distinct histone-modifying enzymes. Recent studies suggest that the four kinds of modifications at H3K27 have inter-correlation in gene transcription or chromatin structure formation.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.6
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• pp.791-797
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• 2018

Objective: Trimethylation of histone 3 (H3) at 4th lysine N-termini (H3K4me3) in gene promoter region was the universal marker of active genes specific to cell lineage. On the contrary, coexistence of trimethylation at 27th lysine (H3K27me3) in the same loci-the bivalent H3K4m3/H3K27me3 was known to suspend the gene transcription in germ cells, and could also be inherited to the developed stem cell. In galline species, throughout example of H3K4m3 and H3K27me3 ChIP-seq analysis was still not provided. We therefore designed and demonstrated such procedures using ChIP-seq and mRNA-seq data of chicken follicular mesenchymal cells and male germ cells. Methods: Analytical workflow was designed and provided in this study. ChIP-seq and RNA-seq datasets of follicular mesenchymal cells and male germ cells were acquired and properly preprocessed. Peak calling by Model-based analysis of ChIP-seq 2 was performed to identify H3K4m3 or H3K27me3 enriched regions ($Fold-change{\geq}2$, $FDR{\leq}0.01$) in gene promoter regions. Integrative genomics viewer was utilized for cellular retinoic acid binding protein 1 (CRABP1), growth differentiation factor 10 (GDF10), and gremlin 1 (GREM1) gene explorations. Results: The acquired results indicated that follicular mesenchymal cells and germ cells shared several unique gene promoter regions enriched with H3K4me3 (5,704 peaks) and also unique regions of bivalent H3K4m3/H3K27me3 shared between all cell types and germ cells (1,909 peaks). Subsequent observation of follicular mesenchyme-specific genes-CRABP1, GDF10, and GREM1 correctly revealed vigorous transcriptions of these genes in follicular mesenchymal cells. As expected, bivalent H3K4m3/H3K27me3 pattern was manifested in gene promoter regions of germ cells, and thus suspended their transcriptions. Conclusion: According the results, an example of chicken H3K4m3/H3K27me3 ChIP-seq data analysis was successfully demonstrated in this study. Hopefully, the provided methodology should hereby be useful for galline ChIP-seq data analysis in the future.

• Genomics & Informatics
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• v.18 no.4
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• pp.42.1-42.9
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• 2020

Chromatin immunoprecipitation coupled with high-throughput DNA sequencing (ChIP-Seq) is a powerful technology to profile the location of proteins of interest on a whole-genome scale. To identify the enrichment location of proteins, many programs and algorithms have been proposed. However, none of the commonly used peak calling programs could accurately explain the binding features of target proteins detected by ChIP-Seq. Here, publicly available data on 12 histone modifications, including H3K4ac/me1/me2/me3, H3K9ac/me3, H3K27ac/me3, H3K36me3, H3K56ac, and H3K79me1/me2, generated from a human embryonic stem cell line (H1), were profiled with five peak callers (CisGenome, MACS1, MACS2, PeakSeq, and SISSRs). The performance of the peak calling programs was compared in terms of reproducibility between replicates, examination of enriched regions to variable sequencing depths, the specificity-to-noise signal, and sensitivity of peak prediction. There were no major differences among peak callers when analyzing point source histone modifications. The peak calling results from histone modifications with low fidelity, such as H3K4ac, H3K56ac, and H3K79me1/me2, showed low performance in all parameters, which indicates that their peak positions might not be located accurately. Our comparative results could provide a helpful guide to choose a suitable peak calling program for specific histone modifications.

• Bulletin of the Korean Chemical Society
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• v.26 no.2
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• pp.233-237
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• 2005

Cyclopentadiene compounds, 2-[CR'R(OMe)]-1,3-Me$_2C_5H_3$ (R, R' = 2,2'-biphenyl, 2) and 2-[CR'R(OSiMe$_3$)]-1,3-Me$_2C_5H_3$ (R, R' = 2,2'-biphenyl, 3; R = ph, R' = ph, 4; R = 2-naphthyl, R' = H, 5) are readily synthesized from 2-bromo-3-methoxy-1,3-dimethylcyclopentene (1). Reaction of the cyclopentadienes with Ti(NMe$_2$)$_4$ in toluene results in clean formation of the cyclopentadienyl tris(dimethylamido)titanium complexes, which are transformed to the trichloride complexes, 2-[CR'R(OMe)]-1,3-Me$_2C_5H_2$}TiCl$_3$ (R, R' = 2,2'-biphenyl, 6) and {2-[CR'R(OSiMe$_3$)]-1,3-Me$_2C_5H_2$}TiCl$_3$ (R, R' = 2,2'-biphenyl, 7; R = ph, R' = ph, 8; R = 2-naphthyl, R' = H, 9). Attempts to form C1-bridged Cp/oxido complexes by elimination of MeCl or Me$_3$SiCl were not successful. X-ray structures of 6, 7 and an intermediate complex {2-[Ph$_2$C(OSiMe$_3$)]-1,3-Me$_2C_5H_2$}TiCl$_2$(NMe$_2$) (10) were determined.

• BMB Reports
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• v.53 no.5
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• pp.266-271
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• 2020

Breast cancer encompasses a major portion of human cancers and must be carefully monitored for appropriate diagnoses and treatments. Among the many types of breast cancers, triple negative breast cancer (TNBC) has the worst prognosis and the least cases reported. To gain a better understanding and a more decisive precursor for TNBC, two major histone modifications, an activating modification H3K4me3 and a repressive modification H3K27me3, were analyzed using data from normal breast cell lines against TNBC cell lines. The combination of these two histone markers on the gene promoter regions showed a great correlation with gene expression. A list of signature genes was defined as active (highly enriched H3K4me3), including NOVA1, NAT8L, and MMP16, and repressive genes (highly enriched H3K27me3), IRX2 and ADRB2, according to the distribution of these histone modifications on the promoter regions. To further enhance the investigation, potential candidates were also compared with other types of breast cancer to identify signs specific to TNBC. RNA-seq data was implemented to confirm and verify gene regulation governed by the histone modifications. Combinations of the biomarkers based on H3K4me3 and H3K27me3 showed the diagnostic value AUC 93.28% with P-value of 1.16e-226. The results of this study suggest that histone modification analysis of opposing histone modifications may be valuable toward developing biomarkers and targets for TNBC.

• Development and Reproduction
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• v.15 no.4
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• pp.273-279
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• 2011

Epigenetic regulation is a phenomenon that changes the gene function without changing the underlying DNA sequences. Epigenetic status of chromosome is regulated by mechanisms such as histone modification, DNA modification, and RNAi silencing. In this review, we focused on histone methylation for epigenetic regulation in ES cells. Two antagonizing multiprotein complexes regulate methylation of histones to guide expression of genes in ES cells. The Polycomb repressive complex 2 (PRC2), including EED, EZH2, and SUZ12 as core factors, contributes to gene repression by increasing trimethylation of H3K27 (H3K27me3). In contrast, the Trithorax group (TrxG) complex including MLL is related to gene activation by making H3K4me3. PRC2 and TrxG accompany a variety of accessory proteins. Most prominent feature of epigenetic regulation in ES cells is a bivalent state in which H3K27me3 and H3K4me3 appear simultaneously. Concerted regulation of PRC2, TrxG complex, and H3K4- or H3K27-specific demethylases activate expression of pluripotency-related genes and suppress development-related genes in ES cells. Modified balance of the regulators also enables ES cells to efficiently differentiate to a variety of cells upon differentiating signals. More detailed insights on the epigenetic regulators and their action will lead us to better understanding and use of ES cells for future application.

• Genomics & Informatics
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• v.10 no.3
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• pp.145-152
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• 2012

Chromatin structure and dynamics that are influenced by epigenetic marks, such as histone modification and DNA methylation, play a crucial role in modulating gene transcription. To understand the relationship between histone modifications and regulatory elements in breast cancer cells, we compared our chromatin immunoprecipitation sequencing (ChIP-Seq) histone modification patterns for histone H3K4me1, H3K4me3, H3K9/16ac, and H3K27me3 in MCF-7 cells with publicly available formaldehyde-assisted isolation of regulatory elements (FAIRE)-chip signals in human chromosomes 8, 11, and 12, identified by a method called FAIRE. Active regulatory elements defined by FAIRE were highly associated with active histone modifications, like H3K4me3 and H3K9/16ac, especially near transcription start sites. The H3K9/16ac-enriched genes that overlapped with FAIRE signals (FAIRE-H3K9/14ac) were moderately correlated with gene expression levels. We also identified functional sequence motifs at H3K4me1-enriched FAIRE sites upstream of putative promoters, suggesting that regulatory elements could be associated with H3K4me1 to be regarded as distal regulatory elements. Our results might provide an insight into epigenetic regulatory mechanisms explaining the association of histone modifications with open chromatin structure in breast cancer cells.

• Korean Journal of Soil Science and Fertilizer
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• v.22 no.4
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• pp.271-279
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• 1989

Mean values representing the particle size distribution and some chemical properties for the cultivated soils were obtained from the analysis results of the typical profiles, which were described by the detailed soil maps throughout Korea. Analysis results of 5,215 soil samples (3,075 for paddy and 2,140 for upland) were available for the determination of mean values. The results are under. 1. Paddy topsoil contained 20.4% for clay, 5.8 for pH, 2.6% for organic matter, 10.4me/100g for exchangeable K, and 89ppm for available $P_2O_5$. Upland topsoil did 17.3% for clay, 5.5 for pH, 1.8% for organic matter, 9.lme/100g for CEC, 0.29me/100g for exchangeable K, and 103ppm for availabal $P_2O_5$. 2. Soil properies for paddy were markedly influenced by the reliefs. Topsoil contained 21.4% for clay, 6.0 for pH, 2.2% for organic matter, 10.8me/100g for CEC, 0.39me/100g for exchang-cable K and 57ppm for available $P_2O_5$ on the fluvio-marine plain, 15.3%, 5.7, 2.0%, 8.6me/100g, 0.17me/100g and 76ppm on the alluvial plain, 18.8%, 5.9, 2.7%, 10.4me/100g, 0.19me/100g and 80ppm on the valleys and fans, 25.0%, 5.7, 2.5%, 11.5me/100g, 0.26me/100g, 0.27me/100g and 141ppm on the moutain foot slopes, respectively. 3. Soil Properties for upland, also, were markedly influenced by the reliefs. Topsoil contained 5.5% for clay, 5.7 for pH, 1.1% for organic matter, 4.7me/100g for CEC, 0.17me/100g for exchangeable K and 50ppm for available $P_2O_5$ on the fluvio-marine plain, 10.3%, 5.5, 1.4%, 7.6me/100g, 0.26me/100g and 160ppm on the alluvial plain, 13.9%, 5.4, 1.8%, 9.3me/100g, 0.24me/100g and and 184ppm on the valleys and fans, 29.8%, 5.3, 2.1%, 11.2me/100g 0.40me/100g and 58ppm on the alluvial plain, 20.0%, 5.7, 2.7%, 11.4me/100g, 0.32me/100g and 116ppm on the mountain foot slopes, and 24.6%, 5.3, 1.8%, 10.2me/100g, 0.28me/100g and 51ppm on the rolling and Hill. 4. All chemical properties did not reach the ideal value for maximizing land capability. 5. Organic matter, exchangeable cations and available $P_2O_5$ were not normally distributed. Intervals of one and two standard deviations about mean of an approximately normal distribution were calculated.

• Bulletin of the Korean Chemical Society
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• v.20 no.1
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• pp.85-88
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• 1999

Me3NO selectively abstracts the proton from [IrH(CO)(PPh3)2L(A)]0.1+,2+ (1) (A: -CCPh, Cl-, CH3CN and L: CH3CN, Cl-, C1O4-) to give the trans-elimination products, Ir(CO)(PPh3)2(A) (2). The reductive elimination of H+ and Cl- from Ir(H)Cl2(CO)(PPh3)2 (lb) to give IrCl(CO)(PPh3)2 (2b) is first order in both lb and Me3NO. The rate law d[2b]/dt=kobs[lb]=k2[lb][Me3NO] suggests the formation of (PPh3)2(CI)2(CO)Ir-H-ON+Me3 in the rate determining step (k2) followed by the fast dissociation of both H-ON+Me3 and the trans ligand Cl-. The rate significantly varies with the cis liaand A and the trans ligand L and is slower with both A and L being Cl- than other ligands. Me3NO selectively eliminates CO from [Ir(H)2(CO)(PPh3)2L]0,+ (3) (L=CH3CN, C1O4-) to produce [Ir(H)2(PPh3)2L'(CH3CN)]+ (4) (L'=CH3CN, PPh3) in the presence of L. Me3NO does not readily remove either H+ or CO from cis, trans- and trans, trans-lr(H)(-CCPh)2(CO)(PPh3)2 and cis, trans-Ir(H)2Cl(CO)(PPh3)2. The choice whether hydridocarbonyls, 1 and 3 undergo the deprotonation or decarbonylation may be understood mostly in terms of thermodynamic stability of the products and partly by kinetic preference of Me3NO on proton and CO.

• Journal of Life Science
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• v.25 no.6
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• pp.703-708
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• 2015

Hox genes encode a highly conserved family of homeodomain-containing transcription factors controlling vertebrate pattern formation along the anteroposterior body axis during embryogenesis. Retinoic acid (RA) is a key morphogen in embryogenesis and a critical regulator of both adult and embryonic cellular activity. Specifically, RA regulates Hox gene expression in mouse- or human-derived embryonic carcinoma (EC) cells. Histone modification has been reported to play a pivotal role in the process of RA-induced gene expression and cell differentiation. As histone modification is thought to play an essential role in RA-induced Hox gene expression, we examined RA-induced initiation of collinear expression of Hox genes and the corresponding histone modifications in F9 murine embryonic teratocarcinoma (EC) cells. Hox expression patterns and histone modifications were analyzed by semiquantitative RT-PCR, RNA-sequencing, and chromatin immuno-precipitation (ChIP)-PCR analyses. The Hoxc4 gene (D0) was initiated earlier than the Hoxc5 to –c10 genes (D3) upon RA treatment (day 0 [D0], day 1 [D1], and day 3 [D3]). The Hox nonexpressing D0 sample had a strong repressive marker, H3K27me3, than the D1 and D3 samples. In the D1 and D3 samples, reduced enrichment of the H3K27me3 marker was observed in the whole cluster. The active H3K4me3 marker was closely associated with the collinear expression of Hoxc genes. Thus, the Hoxc4 gene (D1) and all Hoxc genes (D3) expressed H3K4me3 upon transcription activation. In conclusion, these data indicated that removing H3K27me3 and acquiring H3K4me3 regulated RA-induced Hoxc gene collinearity in F9 cells.