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PRC2-mediated H3K27me3 contributes to transcriptional regulation of FIT-mediated iron deficiency response

ABSTRACT: PRC2-mediated H3K27me3 contributes to transcriptional regulation of FIT-mediated iron deficiency response

PROVIDER: PRJNA523248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8592610_1.fastq.gz	Fastqsanger.gz
	SRR8592610_2.fastq.gz	Fastqsanger.gz
	SRR8592601_1.fastq.gz	Fastqsanger.gz
	SRR8592601_2.fastq.gz	Fastqsanger.gz
	SRR8592611_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

PRC2-mediated H3K27me3 contributes to transcriptional regulation of FIT-mediated iron deficiency response

Project description:We report that H3K27me3 attenuates the induction of FIT-target genes under iron deficiency response

2019-05-15 | GSE126782 | GEO

PRC2-Mediated H3K27me3 Contributes to Transcriptional Regulation of FIT-Dependent Iron Deficiency Response.

Project description:Iron is an essential micronutrient for nearly all organisms, but excessive iron can lead to the formation of cytotoxic reactive oxygen species. Therefore, iron acquisition and homeostasis must be tightly regulated. Plants have evolved complex mechanisms to optimize their use of iron, which is one of the most limiting nutrients in the soil. In particular, transcriptional regulation is vital for regulating iron in plants, and much work has revealed the role of transcription factors on this front. Our study adds novel insights to the transcriptional regulation of iron homeostasis in plants by showing that chromatin remodeling via histone 3 lysine 27 trimethylation (H3K27me3) modulates the expression of FIT-dependent genes under iron deficiency. We provide evidence that FIT-dependent iron acquisition genes, IRT1 and FRO2, as well as FIT itself are direct targets of PRC2-mediated H3K27me3. In the clf mutant, which lacks the predominant H3K27 tri-methyltransferase, induction of FIT, FRO2, IRT1, and other FIT-regulated genes in roots is significantly higher under iron deficient conditions than in wild type. Furthermore, we observe that clf mutants are more tolerant to iron deficiency than wild type, indicating that gene expression levels appear to be limiting the plants ability to access iron. We propose that H3K27me3 attenuates the induction of FIT-target genes under iron deficiency and hypothesize that this may serve as a mechanism to restrict the maximum level of induction of iron acquisition genes to prevent iron overload.

| S-EPMC6532572 | biostudies-literature

PRC2-mediated H3K27me3 regulates iron homeostasis genes in the shoots of Arabidopsis thaliana

Project description:PRC2-mediated H3K27me3 regulates iron homeostasis genes in the shoots of Arabidopsis thaliana

| PRJNA630230 | ENA

Two distinct functional axes of positive feedback-enforced PRC2 recruitment in mouse embryonic stem cells

Project description:Polycomb Repressive Complex 2 (PRC2) plays an essential role in development by catalysing trimethylation of histone H3 lysine 27 (H3K27me3), resulting in gene repression. PRC2 consists of two sub-complexes, PRC2.1 and PRC2.2, in which the PRC2 core associates with distinct ancillary subunits such as MTF2 and JARID2, respectively. Both MTF2, present in PRC2.1, and JARID2, present in PRC2.2, play a role in core PRC2 recruitment to target genes in mouse embryonic stem cells (mESCs). However, it remains unclear how these distinct sub-complexes cooperate to establish H3K27me3 domains. Here, we combine a range of Polycomb mutant mESCs with chemical inhibition of PRC2 catalytic activity, to systematically dissect their relative contributions to PRC2 binding to target loci. We find that PRC2.1 and PRC2.2 mediate two distinct paths for recruitment, with mutually reinforced binding. Part of the cross-talk between PRC2.1 and PRC2.2 occurs via their catalytic product H3K27me3, which is bound by the PRC2 core-subunit EED, thereby mediating a positive feedback. Strikingly, removal of either JARID2 or H3K27me3 only has a minor effect on PRC2 recruitment, whereas their combined ablation largely attenuates PRC2 recruitment. This strongly suggests an unexpected redundancy between JARID2 and EED-H3K27me3-mediated recruitment of PRC2. Furthermore, we demonstrate that all core PRC2 recruitment occurs through the combined action of MTF2-mediated recruitment of PRC2.1 to DNA and PRC1-mediated recruitment of JARID2-containing PRC2.2. Both axes of binding are supported by EED-H3K27me3 positive feedback, but to a different degree. Finally, we provide evidence that PRC1 and PRC2 mutually reinforce reciprocal binding. Together, these data disentangle the interdependent and cooperative interactions between Polycomb complexes that are important to establish Polycomb repression at target sites.

2021-09-22 | PXD020684 | Pride

Two distinct functional axes of positive feedback-enforced PRC2 recruitment in mouse embryonic stem cells

2020-08-07 | PXD014290 | Pride

Interplay between Nsd1 and PRC2 demarcates regions of H3K27me2 and H3K27me3

Project description:The core Polycomb Repressor Complex 2 (PRC2) is composed of Ezh1/2, Suz12, Eed and is responsible for mediating both H3K27me2 and H3K27me3. However, the mechanisms by which PRC2 demarcates these two repressive modifications in the genome are unknown. In a functional screen, we identified the H3K36 dimethyltransferase Nsd1 as a modulator of PRC2-mediated di- and trimethylation of H3K27. ChIP-Seq analysis following the depletion of Nsd1 revealed a global reduction in H3K36me2 and an increase in H3K27me3 at sites previously marked by H3K27me2. We show that the H3K36me2 at H3K27me2 marks co-occupy regions and provide evidence that the presence of H3K36me2 functions to restrict the spatial distribution of Polycomb mediated H3K27me3 domains.

2018-09-15 | GSE86925 | GEO

Interplay between Nsd1 and PRC2 demarcates regions of H3K27me2 and H3K27me3.

2018-03-29 | GSE107773 | GEO

fe-fit-diff_6d-Differential gene expression in A. thaliana roots depending on iron supply and FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) abundance

Project description:au15-01_iron-fit - fe-fit-diff_6d - Changes in gene expression profiles between fit knock-out, wild-type and FIT overexpressor seedlings under sufficient iron supply and under iron deficiency. - Col-0, HA-FIT and fit-3.

2016-07-01 | GSE80281 | GEO

fe-fit-diff_6d-Differential gene expression in A. thaliana roots depending on iron supply and FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) abundance

2016-07-01 | E-GEOD-80281 | biostudies-arrayexpress

Determine the chromatin association change of H3K27me3 and PRC2 in response to PRC2 subtype change or stable CTR9 KD in MCF7 cells

Project description:CTR9 is the scaffold subunit in PAFc (Polymerase associated factor complex), a multifunctional complex employed in multiple steps of RNA Pol II-mediated transcription. CTR9/PAFc is well known as an evolutionarily conserved elongation factor regulating gene activation via coupling with histone modifications enzymes. However, little is known about its function to restrain repressive histone markers. Using inducible and stable CTR9 knockdown breast cancer cell lines, we discovered that the amount of H3K27me3 is strictly controlled by CTR9. Quantitative profiling on histone modifications revealed a striking increase of H3K27me3 level upon loss of CTR9. Moreover, loss of CTR9 leads to genome-wide expansion of H3K27me3, as well as increased recruitment of PRC2 on chromatin, which can be reversed by CTR9 restoration. Moreover, CTR9 depletion triggers a PRC2 subtype switch from less active PRC2.2 to PRC2.1 with higher methyltransferase activity. As a consequence, CTR9 depletion generates vulnerability that renders breast cancer cells hypersensitive to PRC2 inhibitors. Our findings that CTR9 demarcates PRC2-mediated H3K27me3 levels and genomic distribution provide a unique mechanism of transition from transcriptionally active to repressive chromatin states and shed light on the biological functions of CTR9 in development and cancer.

2021-12-02 | GSE189796 | GEO

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