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A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE198182 | GEO | 2023/01/20

REPOSITORIES: GEO

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A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [Micro-C]

Project description:Antibody class switch recombination (CSR) requires the ligation of DNA breaks in transcribed and juxtaposed donor and acceptor switch (S) sequences (S-S synapsis) spaced 50-200 kb apart within the immunoglobulin heavy chain locus (Igh). CSR is believed to occur via the association of active S regions with the 3’ regulatory region (3’RR) super-enhancer thereby coupling transcription with S-S synapsis. Here, we map the multi-way interactome underlying CSR using Tri-C. Surprisingly, S-S synapsis is strongly associated with the 3` CTCF binding element (3`CBE), but not the 3’RR, a finding also confirmed by Micro-C measurements. Instead, the 3’RR forms a self-interacting domain independently engaging with Igh genes. Additionally, transcription at acceptor S regions creates a topological barrier that insulates S-S synapsis from loop extrusion complexes. Thus, Igh gene activation and S-S synapsis occur via distinct topological states created by the interaction between transcription and the loop extrusion machinery.

2023-01-20 | GSE198181 | GEO

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [PRO-seq]

2023-01-20 | GSE198180 | GEO

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [Tri-C]

2023-01-20 | GSE198179 | GEO

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [ChIP-Seq]

2023-01-20 | GSE198176 | GEO

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination

Project description:A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination

| PRJNA814063 | ENA

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [ChIP-Seq]

Project description:A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [ChIP-Seq]

| PRJNA814071 | ENA

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [PRO-seq]

Project description:A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [PRO-seq]

| PRJNA814069 | ENA

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [Micro-C]

Project description:A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [Micro-C]

| PRJNA814068 | ENA

A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [Tri-C]

Project description:A de novo transcription-dependent TAD boundary underpins critical multiway interactions during antibody class switch recombination [Tri-C]

| PRJNA814070 | ENA

De novo protein synthesis is required for the activation-induced cytidine deaminase function in class-switch recombination.

Project description:Activation-induced cytidine deaminase (AID) is required for class-switch recombination (CSR), somatic hypermutation, and gene conversion of Ig genes. Although AID has sequence similarity to an RNA-editing enzyme Apobec-1, how AID functions in CSR and somatic hypermutation is unknown. Because involvement of RNA-editing but not DNA-editing in CSR requires de novo protein synthesis after AID expression, we examined whether protein synthesis inhibitors could block CSR in the presence of the AID activity. For this purpose we constructed AID fused with the hormone-binding domain of the estrogen receptor (AID-ER), which was introduced into AID-deficient spleen B cells. When such transfectants were treated with an estrogen analogue, 4-hydroxytamoxifen (OHT), CSR was induced within 1 h. Cycloheximide or puromycin drastically suppressed OHT-induced CSR in AID-ER expressing AID-/- B cells when added 1 h before OHT but not after OHT, suggesting that de novo protein synthesis is required for an event downstream to AID expression in CSR. The results lend the weight to RNA-editing hypothesis for the function of AID.

| S-EPMC151392 | biostudies-literature

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