scholarly journals A role for MED14 and UVH6 in heterochromatin transcription upon destabilization of silencing

2018 ◽  
Vol 1 (6) ◽  
pp. e201800197 ◽  
Author(s):  
Pierre Bourguet ◽  
Stève de Bossoreille ◽  
Leticia López-González ◽  
Marie-Noëlle Pouch-Pélissier ◽  
Ángeles Gómez-Zambrano ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Environmental Changes ◽  
Constitutive Heterochromatin ◽  
Transcriptional Silencing ◽  
Epigenetic Marks ◽  
Transcriptional Changes ◽  
Heterochromatin Silencing ◽  
Insight Into

Constitutive heterochromatin is associated with repressive epigenetic modifications of histones and DNA which silence transcription. Yet, particular mutations or environmental changes can destabilize heterochromatin-associated silencing without noticeable changes in repressive epigenetic marks. Factors allowing transcription in this nonpermissive chromatin context remain poorly known. Here, we show that the transcription factor IIH component UVH6 and the mediator subunit MED14 are both required for heat stress–induced transcriptional changes and release of heterochromatin transcriptional silencing in Arabidopsis thaliana. We find that MED14, but not UVH6, is required for transcription when heterochromatin silencing is destabilized in the absence of stress through mutating the MOM1 silencing factor. In this case, our results raise the possibility that transcription dependency over MED14 might require intact patterns of repressive epigenetic marks. We also uncover that MED14 regulates DNA methylation in non-CG contexts at a subset of RNA-directed DNA methylation target loci. These findings provide insight into the control of heterochromatin transcription upon silencing destabilization and identify MED14 as a regulator of DNA methylation.

scholarly journals Differential requirement of MED14 and UVH6 for heterochromatin transcription upon destabilization of silencing

2018 ◽  
Author(s):  
Pierre Bourguet ◽  
Stève de Bossoreille ◽  
Leticia López-González ◽  
Marie-Noëlle Pouch-Pélissier ◽  
Ángeles Gómez-Zambrano ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Heat Stress ◽  
Environmental Changes ◽  
Constitutive Heterochromatin ◽  
Epigenetic Marks ◽  
Two Factors ◽  
Silencing Pathways ◽  
Heterochromatin Silencing ◽  
Insight Into ◽  
Chromatin Patterns

AbstractConstitutive heterochromatin is commonly associated with high levels of repressive epigenetic marks and is stably maintained transcriptionally silent by the concerted action of different, yet convergent, silencing pathways. Reactivation of heterochromatin transcription is generally associated with alterations in levels of these epigenetic marks. However, in mutants for particular epigenetic regulators, or upon particular environmental changes such as heat stress, heterochromatin-associated silencing is destabilized without noticeable changes in epigenetic marks. This suggests that transcription can occur in a non-permissive chromatin context, yet the factors involved remain poorly known. Here, we show that heat stress-induced transcription of heterochromatin depends on the TFIIH component UVH6 and the Mediator subunit MED14. Mutants for these two factors exhibit hypersensitivity to heat stress, and under these conditions, UVH6 and MED14 are required for transcription of a high number of loci. We further show that MED14, but not UVH6, is required for transcription when heterochromatin silencing is destabilized in the absence of stress. In this case, MED14 requires proper chromatin patterns of repressive epigenetic marks for its function. We also uncover that MED14 regulates non-CG DNA methylation at a subset of RNA-directed DNA methylation target loci. These findings provide insight into the control of heterochromatin transcription upon silencing destabilization and identify MED14 as a regulator of DNA methylation.

scholarly journals Epigenetic marks of Insulin‐related transcription factor network by DNA methylation

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Shuhei Ito ◽  
Shinya Sato ◽  
Tetsuya Yoshioka ◽  
Jun Ohgane ◽  
Satoshi Tanaka ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Transcription Factor ◽  
Epigenetic Marks ◽  
Transcription Factor Network ◽  
Related Transcription Factor

scholarly journals SLIM1 Transcription Factor Promotes Sulfate Uptake and Distribution to Shoot, Along with Phytochelatin Accumulation, Under Cadmium Stress in Arabidopsis thaliana

Plants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 163 ◽  
Author(s):  
Chisato Yamaguchi ◽  
Soudthedlath Khamsalath ◽  
Yuki Takimoto ◽  
Akiko Suyama ◽  
Yuki Mori ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Transcriptional Regulation ◽  
Cadmium Stress ◽  
Parental Line ◽  
Fresh Weight ◽  
Sulfate Uptake ◽  
S Deficiency ◽  
Transcriptional Changes ◽  
Cd Exposure

Sulfur (S) assimilation, which is initiated by sulfate uptake, generates cysteine, the substrate for glutathione (GSH) and phytochelatin (PC) synthesis. GSH and PC contribute to cadmium (Cd) detoxification by capturing it for sequestration. Although Cd exposure is known to induce the expression of S-assimilating enzyme genes, including sulfate transporters (SULTRs), mechanisms of their transcriptional regulation are not well understood. Transcription factor SLIM1 controls transcriptional changes during S deficiency (−S) in Arabidopsis thaliana. We examined the potential involvement of SLIM1 in inducing the S assimilation pathway and PC accumulation. Cd treatment reduced the shoot fresh weight in the sulfur limitation1 (slim1) mutant but not in the parental line (1;2PGN). Cd-induced increases of sulfate uptake and SULTR1;2 expressions were diminished in the slim1 mutant, suggesting that SLIM1 is involved in inducing sulfate uptake during Cd exposure. The GSH and PC levels were lower in slim1 than in the parental line, indicating that SLIM1 was required for increasing PC during Cd treatment. Hence, SLIM1 indirectly contributes to Cd tolerance of plants by inducing −S responses in the cell caused by depleting the GSH pool, which is consumed by enhanced PC synthesis and sequestration to the vacuole.

scholarly journals Excess light priming in Arabidopsis thaliana genotypes with altered DNA methylomes

2018 ◽  
Author(s):  
Diep R. Ganguly ◽  
Bethany A. B. Stone ◽  
Andrew F. Bowerman ◽  
Steven R. Eichten ◽  
Barry J. Pogson
Keyword(s):  
Dna Methylation ◽  
Arabidopsis Thaliana ◽  
Light Stress ◽  
Preliminary Evidence ◽  
Potential Contribution ◽  
Transcriptional Alterations ◽  
Transcriptional Changes ◽  
Future Events ◽  
Excess Light ◽  
Translational Mechanisms

AbstractPlants must continuously react to the ever-fluctuating nature of their environment. Repeated exposure to stressful conditions can lead to priming, whereby prior encounters heighten a plant’s ability to respond to future events. A clear example of priming is provided by the model plant Arabidopsis thaliana (Arabidopsis), in which photosynthetic and photoprotective responses are enhanced following recurring light stress. While there are various post-translational mechanisms underpinning photoprotection, an unresolved question is the relative importance of transcriptional changes towards stress priming and, consequently, the potential contribution from DNA methylation – a heritable chemical modification of DNA capable of influencing gene expression. Here, we systematically investigate the potential molecular underpinnings of physiological priming against recurring excess-light (EL), specifically DNA methylation and transcriptional regulation: the latter having not been examined with respect to EL priming. The capacity for physiological priming of photosynthetic and photoprotective parameters following a recurring EL treatment was not impaired in Arabidopsis mutants with perturbed establishment, maintenance, or removal of DNA methylation. Importantly, no differences in development or basal photoprotective capacity were identified in the mutants that may confound the above result. Little evidence for a causal transcriptional component of physiological priming was identified; in fact, most alterations in primed plants presented as a transcriptional ‘dampening’ in response to an additional EL exposure, likely a consequence of physiological priming. However, a set of transcripts uniquely regulated in primed plants provide preliminary evidence for a novel transcriptional component of recurring EL priming, independent of physiological changes. Thus, we propose that physiological priming of recurring EL in Arabidopsis occurs independently of DNA methylation; and that the majority of the associated transcriptional alterations are a consequence, not cause, of this physiological priming.One sentence summaryPhotoprotection and priming against recurring excess light is functional despite impaired maintenance of the DNA methylome.

scholarly journals Heterochromatin is a quantitative trait associated with spontaneous epiallele formation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yinwen Zhang ◽  
Hosung Jang ◽  
Rui Xiao ◽  
Ioanna Kakoulidou ◽  
Robert S. Piecyk ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Arabidopsis Thaliana ◽  
Recombinant Inbred Lines ◽  
Three Dimensional ◽  
Feedback Regulation ◽  
Inbred Lines ◽  
Single Base ◽  
Plant Genomes ◽  
Single Base Resolution ◽  
Heterochromatin Silencing

AbstractEpialleles are meiotically heritable variations in expression states that are independent from changes in DNA sequence. Although they are common in plant genomes, their molecular origins are unknown. Here we show, using mutant and experimental populations, that epialleles in Arabidopsis thaliana that result from ectopic hypermethylation are due to feedback regulation of pathways that primarily function to maintain DNA methylation at heterochromatin. Perturbations to maintenance of heterochromatin methylation leads to feedback regulation of DNA methylation in genes. Using single base resolution methylomes from epigenetic recombinant inbred lines (epiRIL), we show that epiallelic variation is abundant in euchromatin, yet, associates with QTL primarily in heterochromatin regions. Mapping three-dimensional chromatin contacts shows that genes that are hotspots for ectopic hypermethylation have increases in contact frequencies with regions possessing H3K9me2. Altogether, these data show that feedback regulation of pathways that have evolved to maintain heterochromatin silencing leads to the origins of spontaneous hypermethylated epialleles.

scholarly journals The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Dongming Li ◽  
Ana Marie S Palanca ◽  
So Youn Won ◽  
Lei Gao ◽  
Ying Feng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Arabidopsis Thaliana ◽  
Gene Silencing ◽  
Methylation Status ◽  
Transcriptional Silencing ◽  
Binding Domain ◽  
Number Of Factors ◽  
Genome Wide ◽  
Eukaryotic Organisms

DNA methylation is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation are known, relatively little is understood about how DNA methylation influences gene expression. Here we identified a METHYL-CpG-BINDING DOMAIN 7 (MBD7) complex in Arabidopsis thaliana that suppresses the transcriptional silencing of two LUCIFERASE (LUC) reporters via a mechanism that is largely downstream of DNA methylation. Although mutations in components of the MBD7 complex resulted in modest increases in DNA methylation concomitant with decreased LUC expression, we found that these hyper-methylation and gene expression phenotypes can be genetically uncoupled. This finding, along with genome-wide profiling experiments showing minimal changes in DNA methylation upon disruption of the MBD7 complex, places the MBD7 complex amongst a small number of factors acting downstream of DNA methylation. This complex, however, is unique as it functions to suppress, rather than enforce, DNA methylation-mediated gene silencing.

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