Identification of AtHD2C as a novel regulator of abscisic acid responses in Arabidopsis

HD2 proteins are plant-specific histone deacetylases. Little is known about the function of HD2 proteins in plants. In this paper, we report that an Arabidopsis HD2 protein, AtHD2C, is involved in abscisic acid and abiotic stress responses. Analysis of Arabidopsis plants containing the AtHD2C:beta-glucuronidase fusion gene revealed that AtHD2C was constitutive expressed in plants. Furthermore, expression of AtHD2C was repressed by abscisic acid. Over-expression of 35S:AtHD2C-GFP in transgenic Arabidopsis plants conferred an abscisic acid-insensitive phenotype. In addition, 35S:AtHD2C-GFP transgenic plants displayed reduced transpiration and enhanced tolerance to salt and drought stresses when compared with wild-type plants. The expression of several abscisic acid-responsive genes was affected in the 35S:AtHD2C-GFP plants. Our study provides evidence indicating that AtHD2C can modulate abscisic acid and stress responses.     

Dynamic Histone Acetylation of Late Embryonic Genes during Seed Germination

Histone acetylation is involved in the regulation of gene expression in plants and eukaryotes. Histone deacetylases (HDACs) are enzymes that catalyze the removal of acetyl groups from histones, which is associated with the repression of gene expression. To study the role of histone acetylation in the regulation of gene expression during seed germination, trichostatin A (TSA), a specific inhibitor of histone deacetylase, was used to treat imbibing Arabidopsis thaliana seeds. GeneChip arrays were used to show that TSA induces up-regulation of 45 genes and down-regulation of 27 genes during seed germination. Eight TSA-up-regulated genes were selected for further analysis – RAB18, RD29B, ATEM1, HSP70 and four late embryogenesis abundant protein genes (LEA). A gene expression time course shows that these eight genes are expressed at high levels in the dry seed and repressed upon seed imbibition at an exponential rate. In the presence of TSA, the onset of repression of the eight genes is not affected but the final level of repressed expression is elevated. Chromatin immunoprecipitation and HDAC assays show that there is a transient histone deacetylation event during seed germination at 1 day after imbibition, which serves as a key developmental signal that affects the repression of the eight genes. Electronic supplementary material Electronic supplementary material is available for this article at and accessible for authorised users.     

UBIQUITIN-SPECIFIC PROTEASE 26 is required for seed development and the repression of PHERES1 in Arabidopsis

The Arabidopsis mutant Atubp26 initiates autonomous endosperm at a frequency of approximately 1% in the absence of fertilization and develops arrested seeds at a frequency of approximately 65% when self-pollinated. These phenotypes are similar to those of the FERTILIZATION INDEPENDENT SEED (FIS) class mutants, mea, fis2, fie, and Atmsi1, which also show development of the central cell into endosperm in the absence of fertilization and arrest of the embryo following fertilization. Atubp26 results from a T-DNA insertion in the UBIQUITIN-SPECIFIC PROTEASE gene AtUBP26, which catalyzes deubiquitination of histone H2B and is required for heterochromatin silencing. The paternal copy of AtUBP26 is able to complement the loss of function of the maternal copy in postfertilization seed development. This contrasts to the fis class mutants where the paternal FIS copy does not rescue aborted seeds. As in the fis class mutants, the Polycomb group (PcG) complex target gene PHERES1 (PHE1) is expressed at higher levels in Atubp26 ovules than in wild type; there is a lower level of H3K27me3 at the PHE1 locus. The phenotypes suggest that AtUBP26 is required for normal seed development and the repression of PHE1.     

The Polycomb group protein MEDEA and the DNA methyltransferase MET1 interact to repress autonomous endosperm development in Arabidopsis

In flowering plants, double fertilization of the female gametes, the egg and the central cell, initiates seed development to give rise to a diploid embryo and the triploid endosperm. In the absence of fertilization, the FERTILIZATION‐INDEPENDENT SEED Polycomb Repressive Complex 2 (FIS‐PRC2) represses this developmental process by histone methylation of certain target genes. The FERTILIZATION‐INDEPENDENT SEED (FIS) class genes MEDEA (MEA) and FERTILIZATION‐INDEPENDENT ENDOSPERM (FIE) encode two of the core components of this complex. In addition, DNA methylation establishes and maintains the repression of gene activity, for instance via DNA METHYLTRANSFERASE1 (MET1), which maintains methylation of symmetric CpG residues. Here, we demonstrate that Arabidopsis MET1 interacts with MEA in vitro and in a yeast two‐hybrid assay, similar to the previously identified interaction of the mammalian homologues DNMT1 and EZH2. MET1 and MEA share overlapping expression patterns in reproductive tissues before and after fertilization, a prerequisite for an interaction in vivo. Importantly, a much higher percentage of central cells initiate endosperm development in the absence of fertilization in mea‐1/MEA; met1‐3/MET1 as compared to mea‐1/MEA mutant plants. In addition, DNA methylation at the PHERES1 and MEA loci, imprinted target genes of the FIS‐PRC2, was affected in the mea‐1 mutant compared with wild‐type embryos. In conclusion, our data suggest a mechanistic link between two major epigenetic pathways involved in histone and DNA methylation in plants by physical interaction of MET1 with the FIS‐PRC2 core component MEA. This concerted action is relevant for the repression of seed development in the absence of fertilization.     

High-resolution analysis of parent-of-origin allelic expression in the Arabidopsis Endosperm

Genomic imprinting is an epigenetic phenomenon leading to parent-of-origin specific differential expression of maternally and paternally inherited alleles. In plants, genomic imprinting has mainly been observed in the endosperm, an ephemeral triploid tissue derived after fertilization of the diploid central cell with a haploid sperm cell. In an effort to identify novel imprinted genes in Arabidopsis thaliana, we generated deep sequencing RNA profiles of F1 hybrid seeds derived after reciprocal crosses of Arabidopsis Col-0 and Bur-0 accessions. Using polymorphic sites to quantify allele-specific expression levels, we could identify more than 60 genes with potential parent-of-origin specific expression. By analyzing the distribution of DNA methylation and epigenetic marks established by Polycomb group (PcG) proteins using publicly available datasets, we suggest that for maternally expressed genes (MEGs) repression of the paternally inherited alleles largely depends on DNA methylation or PcG-mediated repression, whereas repression of the maternal alleles of paternally expressed genes (PEGs) predominantly depends on PcG proteins. While maternal alleles of MEGs are also targeted by PcG proteins, such targeting does not cause complete repression. Candidate MEGs and PEGs are enriched for cis-proximal transposons, suggesting that transposons might be a driving force for the evolution of imprinted genes in Arabidopsis. In addition, we find that MEGs and PEGs are significantly faster evolving when compared to other genes in the genome. In contrast to the predominant location of mammalian imprinted genes in clusters, cluster formation was only detected for few MEGs and PEGs, suggesting that clustering is not a major requirement for imprinted gene regulation in Arabidopsis.     

组蛋白乙酰化与癌症

由于组蛋白被修饰所引起的染色质结构的改变,在真核生物基因表达调控中发挥着重要的作用,这些修饰主要包括甲基化、乙酰化、磷酸化和泛素化等,其中组蛋白乙酰化尤为重要.组蛋白乙酰转移酶（HAT）和组蛋白去乙酰化酶（HDAC）参与决定组蛋白乙酰化状态.HAT通常作为多亚基辅激活物复合体的一部分,催化组蛋白乙酰化,导致染色质结构的松散、激活转录;而HDAC是多亚基辅抑制物复合体的一部分,使组蛋白去乙酰化,导致染色质集缩,并抑制基因的转录. 编码这些酶的基因染色体易位易于导致急性白血病的发生.另一方面,已经确定了一些乙酰化修饰酶的基因在染色体上的位置,它们尤其倾向定位于染色体的断裂处.综述了HAT和HDAC参与的组蛋白乙酰化与癌症发生之间关系的最新进展,以期进一步阐明组蛋白乙酰化修饰酶的生物学功能以及它们在癌症发生过程中的作用.