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ACD15, ACD21 and SLN regulate accumulation and mobility of MBD6 to silence genes and transposable elements

ABSTRACT: ACD15, ACD21 and SLN regulate accumulation and mobility of MBD6 to silence genes and transposable elements

PROVIDER: PRJNA981636 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24880416_1.fastq.gz	Fastqsanger.gz
	SRR24880416_2.fastq.gz	Fastqsanger.gz
	SRR24880417_1.fastq.gz	Fastqsanger.gz
	SRR24880417_2.fastq.gz	Fastqsanger.gz
	SRR24880418_1.fastq.gz	Fastqsanger.gz

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ACD15, ACD21 and SLN regulate accumulation and mobility of MBD6 to silence genes and transposable elements [ChIP-seq]

Project description:DNA methylation mediates silencing of transposable elements and genes in part via recruitment of the Arabidopsis MBD5/6 complex, which contains the methyl-CpG-binding domain (MBD) proteins MBD5 and MBD6, and the J-domain containing protein SILENZIO (SLN). Here we characterize two additional complex members: α-crystalline domain containing proteins ACD15 and ACD21. We show that they are necessary for gene silencing, bridge SLN to the complex, and promote higher order multimerization of MBD5/6 complexes within heterochromatin. These complexes are also highly dynamic, with the mobility of complex components regulated by the activity of SLN. Using a dCas9 system, we demonstrate that tethering the ACDs to an ectopic site outside of heterochromatin can drive massive accumulation of MBD5/6 complexes into large nuclear bodies. These results demonstrate that ACD15 and ACD21 are critical components of gene silencing complexes that act to drive the formation of higher order, dynamic assemblies.

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Project description:DNA methylation mediates silencing of transposable elements and genes in part via recruitment of the Arabidopsis MBD5/6 complex, which contains the methyl-CpG binding domain (MBD) proteins MBD5 and MBD6, and the J-domain containing protein SILENZIO (SLN). Here, we characterize two additional complex members: α-crystalline domain (ACD) containing proteins ACD15 and ACD21. We show that they are necessary for gene silencing, bridge SLN to the complex, and promote higher-order multimerization of MBD5/6 complexes within heterochromatin. These complexes are also highly dynamic, with the mobility of MBD5/6 complexes regulated by the activity of SLN. Using a dCas9 system, we demonstrate that tethering the ACDs to an ectopic site outside of heterochromatin can drive a massive accumulation of MBD5/6 complexes into large nuclear bodies. These results demonstrate that ACD15 and ACD21 are critical components of the gene-silencing MBD5/6 complex and act to drive the formation of higher-order, dynamic assemblies at CG methylation (meCG) sites.

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