13 research outputs found
Arabidopsis HDA6 Regulates Locus-Directed Heterochromatin Silencing in Cooperation with MET1
Heterochromatin silencing is pivotal for genome stability in eukaryotes. In
Arabidopsis, a plant-specific mechanism called
RNA–directed DNA methylation (RdDM) is involved in heterochromatin
silencing. Histone deacetylase HDA6 has been identified as a component of such
machineries; however, its endogenous targets and the silencing mechanisms have
not been analyzed globally. In this study, we investigated the silencing
mechanism mediated by HDA6. Genome-wide transcript profiling revealed that the
loci silenced by HDA6 carried sequences corresponding to the RDR2-dependent
24-nt siRNAs, however their transcript levels were mostly unaffected in the
rdr2 mutant. Strikingly, we observed significant overlap of
genes silenced by HDA6 to those by the CG DNA methyltransferase MET1.
Furthermore, regardless of dependence on RdDM pathway, HDA6 deficiency resulted
in loss of heterochromatic epigenetic marks and aberrant enrichment for
euchromatic marks at HDA6 direct targets, along with ectopic expression of these
loci. Acetylation levels increased significantly in the hda6
mutant at all of the lysine residues in the H3 and H4 N-tails, except H4K16.
Interestingly, we observed two different CG methylation statuses in the
hda6 mutant. CG methylation was sustained in the
hda6 mutant at some HDA6 target loci that were surrounded
by flanking DNA–methylated regions. In contrast, complete loss of CG
methylation occurred in the hda6 mutant at the HDA6 target loci
that were isolated from flanking DNA methylation. Regardless of CG methylation
status, CHG and CHH methylation were lost and transcriptional derepression
occurred in the hda6 mutant. Furthermore, we show that HDA6
binds only to its target loci, not the flanking methylated DNA, indicating the
profound target specificity of HDA6. We propose that HDA6 regulates
locus-directed heterochromatin silencing in cooperation with MET1, possibly
recruiting MET1 to specific loci, thus forming the foundation of silent
chromatin structure for subsequent non-CG methylation
Epigenetic regulation of gene responsiveness in Arabidopsis
The regulation of chromatin structure is inevitable for proper transcriptional response in eukaryotes. Recent reports in Arabidopsis have suggested that gene responsiveness is modulated by particular chromatin status. One such feature is H2A.Z, a histone variant conserved among eukaryotes. In Arabidopsis, H2A.Z is enriched within gene bodies of transcriptionally variable genes, which is in contrast to genic DNA methylation found within constitutive genes. In the absence of H2A.Z, the genes normally harboring H2A.Z within gene bodies are transcriptionally misregulated, while DNA methylation is unaffected. Therefore, H2A.Z may promote variability of gene expression without affecting genic DNA methylation. Another epigenetic information that could be important for gene responsiveness is trimethylation of histone H3 lysine 4 (H3K4me3). The level of H3K4me3 increases when stress responsive genes are transcriptionally activated, and it decreases after recovery from the stress. Even after the recovery, however, H3K4me3 is kept at some atypical levels, suggesting possible role of H3K4me3 for a stress memory. In this review, we summarize and discuss the growing evidences connecting chromatin features and gene responsiveness
Simple and universal function of acetic acid to overcome the drought crisis
Abstract Acetic acid is a simple and universal compound found in various organisms. Recently, acetic acid was found to play an essential role in conferring tolerance to water deficit stress in plants. This novel mechanism of drought stress tolerance mediated by acetic acid via networks involving phytohormones, genes, and chromatin regulation has great potential for solving the global food crisis and preventing desertification caused by global warming. We highlight the functions of acetic acid in conferring tolerance to water deficit stress
The Cold Signaling Attenuator HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE1 Activates FLOWERING LOCUS C Transcription via Chromatin Remodeling under Short-Term Cold Stress in Arabidopsis
Exposure to short-term cold stress delays flowering by activating the floral repressor FLOWERING LOCUS C (FLC) in Arabidopsis thaliana. The cold signaling attenuator HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE1 (HOS1) negatively regulates cold responses. Notably, HOS1-deficient mutants exhibit early flowering, and FLC expression is suppressed in the mutants. However, it remains unknown how HOS1 regulates FLC expression. Here, we show that HOS1 induces FLC expression by antagonizing the actions of FVE and its interacting partner histone deacetylase 6 (HDA6) under short-term cold stress. HOS1 binds to FLC chromatin in an FVE-dependent manner, and FVE is essential for the HOS1-mediated activation of FLC transcription. HOS1 also interacts with HDA6 and inhibits the binding of HDA6 to FLC chromatin. Intermittent cold treatments induce FLC expression by activating HOS1, which attenuates the activity of HDA6 in silencing FLC chromatin, and the effects of intermittent cold are diminished in hos1 and fve mutants. These observations indicate that HOS1 acts as a chromatin remodeling factor for FLC regulation under short-term cold stress
Genome-Wide Negative Feedback Drives Transgenerational DNA Methylation Dynamics in Arabidopsis
International audienc
Effects of disrupted heterochromatin in the <i>DDM1</i> wild type background examined at single base resolution.
<p>(A) Methylation level was compared for each transcription unit in CG, CHG, and CHH contexts. The format is as shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.g002" target="_blank">Fig 2A</a>. A globally hypomethylated epiRIL (epiRIL98: plant #3 in Fig <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.g007" target="_blank">7A</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.g007" target="_blank">7B</a> and plant #2 in Fig <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.g007" target="_blank">7E</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.g007" target="_blank">7F</a>) and two epiRILs with lower level of hypomethylation (epiRIL260 and epiRIL480) are shown. Global hypomethylation indexes of epiRIL98, epiRIL260, and epiRIL480 are 0.38, 0.04, and 0.09, respectively. “WT” data are from the parental wild-type Col plant used to generate the epiRILs. (B) CHG methylation levels in the genes that were not methylated in WT but methylated in epiRIL98 (methylation level < 0.1 in WT and ≥ 0.1 in epiRIL98: n = 232). For these transcription units, distributions of the methylation levels were compared among the parental WT, the parental 4G <i>ddm1</i> plant, and the epiRIL98. (C-D) Ectopic CHG methylation in epiRIL98 compared to wild type. Each gene was assigned to the inferred haplotypes in epiRIL98: WT-like (C) or <i>ddm1</i>-like (D). The ectopic methylation could be detected in genes of the WT-like haplotype. Examples of such genes are shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.s027" target="_blank">S25 Fig</a>.</p
A model for the transgenerational heterochromatin redistribution.
<p>The cylinder indicates a nucleosome. Red dots above the nucleosome indicate methylation of H3K9. Red and blue lines indicate DNA with and without non-CG methylation, respectively. The CMTs are non-CG methylases, such as CMT3 and CMT2 [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.ref010" target="_blank">10</a>,<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.ref011" target="_blank">11</a>]. SUVHs are H3K9 methylases, such as SUVH4/KYP, SUVH5 and SUVH6 [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.ref075" target="_blank">75</a>]. In both WT and <i>ddm1</i> mutant plants, the histone demethylase IBM1 removes H3K9me from transcribed genes.</p
Hypermethylated regions in <i>ddm1</i> and <i>ibm1</i> mutants.
<p>(A) Increase of CHG methylation in 1G and 3G <i>ibm1</i> mutants. Genes hypermethylated in 1G <i>ibm1</i> (CHG methylation level < 0.1 in WT and ≥ 0.1 in 1G <i>ibm1</i>) are shown (right) with total genes (left). Profiles for multiple 1G and 3G <i>ibm1</i> mutant plants are shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.s017" target="_blank">S15 Fig</a>. (B) Comparison of regions CHG hypermethylated in <i>ibm1</i> and 9G <i>ddm1</i>. DMRs between 9G and 1G <i>ddm1</i> (blue), between 1G <i>ibm1</i> and WT (orange), and between 3G <i>ibm1</i> and WT (red) are shown. Heat map of CHG methylation for these DMRs are shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.s018" target="_blank">S16B Fig</a>. (C) DNA methylation profile for the genes CHG hyper-methylated in 9G <i>ddm1</i> (shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005154#pgen.1005154.g003" target="_blank">Fig 3D</a>). The top and bottom half represent genes and TEGs, respectively. In these regions, CHH methylation also increased in 9G <i>ddm1</i>.</p