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Partitioning of the maize epigenome by the number of methyl groups on histone H3 lysines 9 and 27
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We report a detailed analysis of maize chromosome structure with respect to seven histone H3 methylation states (dimethylation at lysine 4 and mono-, di-, and trimethylation at lysines 9 and 27). Three-dimensional light microscopy and the fine cytological resolution of maize pachytene chromosomes made it possible to compare the distribution of individual histone methylation events to each other and to DNA staining intensity. Major conclusions are that (1) H3K27me2 marks classical heterochromatin; (2) H3K4me2 is limited to areas between and around H3K27me2-marked chromomeres, clearly demarcating the euchromatic gene space; (3) H3K9me2 is restricted to the euchromatic gene space; (4) H3K27me3 occurs in a few (roughly seven) focused euchromatic domains; (5) centromeres and CENP-C are closely associated with H3K9me2 and H3K9me3; and (6) histone H4K20 di- and trimethylation are nearly or completely absent in maize. Each methylation state identifies different regions of the epigenome. We discuss the evolutionary lability of histone methylation profiles and draw a distinction between H3K9me2-mediated gene silencing and heterochromatin formation. 相似文献
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Ji-Yun Shang Xue-Wei Cai Yin-Na Su Zhao-Chen Zhang Xin Wang Nan Zhao Xin-Jian He 《植物学报(英文版)》2022,64(12):2438-2454
Although the Trithorax histone methyltransferases ATX1–5 are known to regulate development and stress responses by catalyzing histone H3K4 methylation in Arabidopsis thaliana, it is unknown whether and how these histone methyltransferases affect DNA methylation. Here, we found that the redundant ATX1–5 proteins are not only required for plant development and viability but also for the regulation of DNA methylation. The expression and H3K4me3 levels of both RNA-directed DNA methylation (RdDM) genes (NRPE1, DCL3, IDN2, and IDP2) and active DNA demethylation genes (ROS1, DML2, and DML3) were downregulated in the atx1/2/4/5 mutant. Consistent with the facts that the active DNA demethylation pathway mediates DNA demethylationmainly at CG and CHG sites, and that the RdDM pathway mediates DNA methylation mainly at CHH sites, whole-genome DNA methylation analyses showed that hyper-CG and CHG DMRs in atx1/2/4/5 significantly overlapped with those in the DNA demethylation pathway mutant ros1 dml2 dml3 (rdd), and that hypo-CHH DMRs in atx1/2/4/5 significantly overlapped with those in the RdDM mutant nrpe1, suggesting that the ATX paralogues function redundantly to regulate DNA methylation by promoting H3K4me3 levels and expression levels of both RdDM genes and active DNA demethylation genes. Given that the ATX proteins function as catalytic subunits of COMPASS histone methyltransferase complexes, we also demonstrated that the COMPASS complex components function as a whole to regulate DNA methylation. This study reveals a previously uncharacterized mechanism underlying the regulation of DNA methylation. 相似文献
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Nady N Lemak A Walker JR Avvakumov GV Kareta MS Achour M Xue S Duan S Allali-Hassani A Zuo X Wang YX Bronner C Chédin F Arrowsmith CH Dhe-Paganon S 《The Journal of biological chemistry》2011,286(27):24300-24311
Histone modifications and DNA methylation represent two layers of heritable epigenetic information that regulate eukaryotic chromatin structure and gene activity. UHRF1 is a unique factor that bridges these two layers; it is required for maintenance DNA methylation at hemimethylated CpG sites, which are specifically recognized through its SRA domain and also interacts with histone H3 trimethylated on lysine 9 (H3K9me3) in an unspecified manner. Here we show that UHRF1 contains a tandem Tudor domain (TTD) that recognizes H3 tail peptides with the heterochromatin-associated modification state of trimethylated lysine 9 and unmodified lysine 4 (H3K4me0/K9me3). Solution NMR and crystallographic data reveal the TTD simultaneously recognizes H3K9me3 through a conserved aromatic cage in the first Tudor subdomain and unmodified H3K4 within a groove between the tandem subdomains. The subdomains undergo a conformational adjustment upon peptide binding, distinct from previously reported mechanisms for dual histone mark recognition. Mutant UHRF1 protein deficient for H3K4me0/K9me3 binding shows altered localization to heterochromatic chromocenters and fails to reduce expression of a target gene, p16(INK4A), when overexpressed. Our results demonstrate a novel recognition mechanism for the combinatorial readout of histone modification states associated with gene silencing and add to the growing evidence for coordination of, and cross-talk between, the modification states of H3K4 and H3K9 in regulation of gene expression. 相似文献
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Deleris A Greenberg MV Ausin I Law RW Moissiard G Schubert D Jacobsen SE 《EMBO reports》2010,11(12):950-955
Histone demethylases-both lysine-specific demethylase 1 (LSD1) and Jumonji-C (JmjC) domain-containing proteins-are broadly implicated in the regulation of chromatin-dependent processes. In Arabidopsis thaliana, histone marks directly affect DNA methylation, and mutations in LSD1 homologues show reduced DNA methylation at some loci. We screened transfer DNA mutations in genes encoding JmjC domains for defects in DNA methylation. Mutations in jmj14 result in reduced DNA methylation in non-CG contexts at targets of DRM2 (domains rearranged methyltransferase 2)-mediated RNA-directed DNA methylation (RdDM), which is associated with an increase in H3K4m3. Unlike other components of RdDM, JMJ14 is not required for de novo methylation of a transgene, suggesting that JMJ14 is specifically involved in the maintenance phase of DRM2-mediated RdDM. 相似文献
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Holocarboxylase synthetase (HLCS) is a chromatin protein that facilitates the creation of histone H3 lysine 9-methylation (H3K9me) gene repression marks through physical interactions with the histone methyltransferase EHMT-1. HLCS knockdown causes a depletion of H3K9me marks in mammalian cell cultures and severe phenotypes such as short lifespan and low stress resistance in Drosophila melanogaster. HLCS displays a punctuate distribution pattern in chromatin despite lacking a strong DNA-binding domain. Previous studies suggest that the binding of HLCS to chromatin depends on DNA methylation. We tested the hypothesis that HLCS interacts physically with the DNA methyltransferase DNMT1 and the methyl CpG binding protein MeCP2 to facilitate the binding of HLCS to chromatin, and that these interactions contribute toward the repression of long-terminal repeats (LTRs) by H3K9me marks. Co-immunoprecipitation and limited proteolysis assays provided evidence suggesting that HLCS interacts physically with both DNMT1 and MeCP2. The abundance of H3K9me marks was 207% greater in the LTR15 locus in HLCS overexpression human embryonic kidney HEK293 cells compared with controls. This gain in H3K9me was inversely linked with a 87% decrease in mRNA coding for LTRs. Effects of HLCS abundance on LTR expression were abolished when DNA methylation marks were erased by treating cells with 5-azacytidine. We conclude that interactions between DNA methylation and HLCS are crucial for mediating gene repression by H3K9me, thereby providing evidence for epigenetic synergies between the protein biotin ligase HLCS and dietary methyl donors. 相似文献
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RNA介导的DNA甲基化作用(RNA-directed DNA Methylation,RdDM)是首次在植物中发现的基因组表观修饰现象,RdDM通过RNA-DNA序列相互作用直接导致DNA甲基化。植物中的RdDM和siRNA介导的mRNA降解现象,都是通过RNA使序列特异性基因发生沉默,它们对于植物的染色体重排、抵御病毒感染、基因表达调控和发育的许多过程起到了非常重要的作用。在植物中有很多的文献报道RdDM现象,但是对于其具体调控机理还不是很清楚。这里对RNA介导的植物DNA甲基化的基本特征进行了简要概述,主要对RdDM机理的研究进展进行了综述,其中包括RdDM过程中的DNA甲基转移酶的种类及其作用机理,DNA甲基化与染色质修饰之间的关系,以及与RdDM相关的重要蛋白质的研究等。在植物中,转录和转录后水平都可能发生RdDM,诱发基因沉默,前者常涉及靶基因启动子的甲基化,后者则牵涉到编码区的甲基化。RdDM的发生依赖于RNAi途径中相似的siRNA和酶,如DCL3、RdR2、SDE4和AGO4。植物中至少含有三类DNA甲基转移酶DRM1/2、MET1和CMT3,其作用部位是与RNA同源的DNA区域中的所有胞嘧啶,而组蛋白H3第九位赖氨酸的甲基化影响着胞嘧啶的甲基化。 相似文献
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Sasaki T Kobayashi A Saze H Kakutani T 《The Plant journal : for cell and molecular biology》2012,70(5):750-758
Methylation of histone H3 lysine 9 (H3K9me) and small RNAs are associated with constitutively silent chromatin in diverse eukaryotes including plants. In plants, silent transposons are also marked by cytosine methylation, especially at non‐CpG sites. Transposon‐specific non‐CpG methylation in plants is controlled by small RNAs and H3K9me. Although it is often assumed that small RNA directs H3K9me, interaction between small RNA and H3K9me has not been directly demonstrated in plants. We have previously shown that a mutation in the chromatin remodeling gene DDM1 (DECREASE IN DNA METHYLATION 1) induces a global decrease but a local increase of cytosine methylation and accumulation of small RNA at a locus called BONSAI. Here we show that de novo BONSAI methylation does not depend on RNAi but does depend on H3K9me. In mutants of H3K9 methyltransferase gene KRYPTONITE or the H3K9me‐dependent DNA methyltransferase gene CHROMOMETHYALSE3, the ddm1‐induced de novo cytosine methylation was abolished for all three contexts (CpG, CpHpG and CpHpH). Furthermore, RNAi mutants showed strong developmental defects when combined with the ddm1 mutation. Our results revealed unexpected interactions of epigenetic modifications that may be conserved among diverse eukaryotes. 相似文献