Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences [GRO-seq]

ABSTRACT: Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences [GRO-seq]

PROVIDER: PRJNA746967 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15150492.fastq.gz	Fastqsanger.gz
	SRR15150493.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences [GRO-seq]

Project description:Somatic hypermutation (SHM) drives the genetic diversity of immunoglobulin genes in activated B cells and supports the generation of antibodies with increased affinity for antigen. SHM is targeted to Ig genes by their enhancers (DIVACs; diversification activators) but how the enhancers mediate this activity is unknown. We show that DIVACs that strongly stimulate SHM increase the phosphorylation of RNA polymerase 2 (Pol2) and Pol2 occupancy in the mutating gene with little or no accompanying increase in elongation-competent Pol2 or production of full length transcripts, indicating the accumulation of stalled Pol2. DIVAC-induced stalling is weakly associated with an increase in the detection of single-stranded DNA bubbles in the mutating target gene. We did not find evidence for anti-sense transcription or an association of H3K27ac with DIVAC activity in the mutating gene. These findings argue for a connection between Pol2 stalling and cis-acting targeting elements in the context of SHM and thus define a mechanistic basis for locus-specific targeting of SHM in the genome. Our results suggest that DIVACs make the target gene a suitable platform for AID-mediated mutation without the need for increasing transcriptional output.

2021-10-22 | GSE180176 | GEO

Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences

Project description:Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences

| PRJNA746964 | ENA

Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences [ChIP-Seq]

2021-10-22 | GSE180177 | GEO

Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences [ChIP-Seq]

Project description:Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences [ChIP-Seq]

| PRJNA746968 | ENA

Immunoglobulin enhancers increase RNA polymerase 2 stalling at somatic hypermutation target sequences

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-10-22 | GSE180178 | GEO

Bach2 regulates AID-mediated immunoglobulin gene conversion and somatic hypermutation in DT40 B cells

Project description:The transcription factor Bach2 is required for germinal center formation and somatic hypermutation (SHM) of immunoglobulins, both central to an efficient antibody-mediated immune response. Activation-induced cytidine deaminase (AID) initiates SHM and CSR in germinal centers and has potential to induce human B cell lymphoma. To understand the role of Bach2 in AID-mediated immunoglobulin gene diversification processes, we established a Bach2-deficient DT40 B cell line. We show that in addition to allowing SHM, Bach2 drives immunoglobulin gene conversion (GCV), an important AID-dependent antibody gene diversification process. We demonstrate that Bach2 promotes GCV by increasing the expression of AID. Importantly, we found that the regulation of AID is independent of Blimp-1 and that Bach2-deficient cells have altered expression of several genes regulating AID expression, stability and function. These results demonstrate that Bach2 has a previously unappreciated role in the production of high-affinity antibodies.

2017-03-27 | GSE92430 | GEO

Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of human MLN B cells.

Project description:Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of human MLN B cells.

| PRJNA1084083 | ENA

Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of mouse splenic B cells.

Project description:Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of mouse splenic B cells.

| PRJNA1084082 | ENA

Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of human tonsil B cells.

Project description:Mutability and hypermutation antagonize immunoglobulin codon optimality Analysis of human tonsil B cells.

| PRJNA1084084 | ENA

Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes

Project description:Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes