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Short tandem repeats are important contributors to silencer elements in T cells

ABSTRACT: Short tandem repeats are important contributors to silencer elements in T cells

PROVIDER: PRJNA836547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19144706_1.fastq.gz	Fastqsanger.gz
	SRR19144706_2.fastq.gz	Fastqsanger.gz
	SRR19144707_1.fastq.gz	Fastqsanger.gz
	SRR19144707_2.fastq.gz	Fastqsanger.gz
	SRR19144708_1.fastq.gz	Fastqsanger.gz

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Project description:More than 25 inherited human disorders are caused by the unstable expansion of repetitive DNA sequences termed short tandem repeats (STRs). A fundamental unresolved question is why some STRs are susceptible to pathologic expansion, whereas thousands of repeat tracts across the human genome are relatively stable. Here, we discover that nearly all disease-associated STRs (daSTRs) are located at boundaries demarcating 3D chromatin domains. We identify a subset of boundaries with markedly higher CpG island density compared to the rest of the genome. daSTRs specifically localize to ultra-high-density CpG island boundaries, suggesting they might be hotspots for epigenetic misregulation or topological disruption upon STR expansion. Fragile X Syndrome (FXS) patients exhibit severe boundary disruption in a manner that correlates with local loss of CTCF occupancy and the degree of FMR1 silencing. Our data uncover higher-order chromatin architecture as a new dimension in understanding repeat expansion disorders.

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Switch tandem repeats influence the choice of the alternative end-joining pathway in class switch recombination

Project description:Switch tandem repeats influence the choice of the alternative end-joining pathway in class switch recombination

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Structural Variant of a Tandem Repeat-containing Silencer Locus Reveals Distinct Pol II and Pol IV-dependent Pathways of siRNA Biogenesis

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