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Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [RNA-seq]

ABSTRACT: Antigen receptor loci are organized into variable (V), diversity (D), and joining (J) elements that rearrange to generate diverse antigen receptor repertoires. Here, we identified an enhancer (E34) in the immunoglobulin kappa locus (Igκ) that instructed rearrangement of Vκ genes located in a sub-topologically associating domain (subTAD), including a Vκ gene encoding for antibodies targeting bacterial phosphorylcholine. E34 promoted the deposition of active histone marks across the E34 subTAD to instruct its nuclear repositioning from a V(D)J recombination-repressive compartment to a permissive one. E34-induced nuclear repositioning of the E34 subTAD promoted Vκ-Jκ interactions assisted by enhancer-associated epigenetic marks and de novo CTCF binding. Finally, we found that E34-instructed Vκ-Jκ rearrangement was essential to combat Streptococcus pneumoniae but not methicillin-resistant Staphylococcus aureus or influenza infections. These data show how enhancer-instructed chromatin topology mechanically pulls specific Vκ and Jκ genes into close physical proximity to generate distinct antibody repertoires to combat bacterial infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE193846 | GEO | 2022/12/05

REPOSITORIES: GEO

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Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [Hi-C]

Project description:Antigen receptor loci are organized into variable (V), diversity (D), and joining (J) elements that rearrange to generate diverse antigen receptor repertoires. Here, we identified an enhancer (E34) in the immunoglobulin kappa locus (Igκ) that instructed rearrangement of Vκ genes located in a sub-topologically associating domain (subTAD), including a Vκ gene encoding for antibodies targeting bacterial phosphorylcholine. E34 promoted the deposition of active histone marks across the E34 subTAD to instruct its nuclear repositioning from a V(D)J recombination-repressive compartment to a permissive one. E34-induced nuclear repositioning of the E34 subTAD promoted Vκ-Jκ interactions assisted by enhancer-associated epigenetic marks and de novo CTCF binding. Finally, we found that E34-instructed Vκ-Jκ rearrangement was essential to combat Streptococcus pneumoniae but not methicillin-resistant Staphylococcus aureus or influenza infections. These data show how enhancer-instructed chromatin topology mechanically pulls specific Vκ and Jκ genes into close physical proximity to generate distinct antibody repertoires to combat bacterial infection.

2022-12-05 | GSE193967 | GEO

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [CUT&RUN]

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Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [ATAC-seq]

2022-12-05 | GSE193813 | GEO

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection

Project description:Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection

| PRJNA798659 | ENA

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [CUT&RUN]

Project description:Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [CUT&RUN]

| PRJNA798041 | ENA

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [ATAC-seq]

Project description:Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [ATAC-seq]

| PRJNA798026 | ENA

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [RNA-seq]

Project description:Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [RNA-seq]

| PRJNA798079 | ENA

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [Hi-C]

Project description:Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [Hi-C]

| PRJNA798665 | ENA

Regulated Capture of Vk Gene Topologically Associating Domains by Transcription Factories

Project description:Antigen receptor gene recombination requires stochastic, monoallelic choice of a single variable gene in each lymphocyte progenitor. However, how this occurs remains unknown. Herein, we report that prior to Vκ to Jκ gene recombination, Igκ alleles reside within spatially different nuclear niches defined by elongating RNA Polymerase II (e-Pol II) and cyclin D3 complexes assembled on the nuclear matrix. Upon cell cycle exit, and cyclin D3 downregulation, only the Vκ allele in the more constrained e-Pol II niche was transcribed. Chromatin modeling and single cell RNA-seq revealed that the nuclear niche favored Vκ flanking CTCF sites, thus shaping the transcribed repertoire. Furthermore, multiple contiguous Vκs oriented away from CTCF sites were preferentially transcribed. Cyclin D3 also repressed monoallelic protocadherin and olfactory genes. These studies of Igκ reveal a general mechanism by which regulated, stochastic chromatin loop capture by fixed e-Pol II complexes generates diversity and couples cell cycle exit to monogenic choice.

2018-08-08 | GSE84705 | GEO

TNFalpha signaling primes chromatin for NF-kappaB binding and induces rapid and widespread nucleosome repositioning

Project description:Background The rearrangement of nucleosomes along the DNA fiber profoundly affects gene expression, but little is known about how signaling reshapes the chromatin landscape, in 3D space and over time, to allow the establishment of new transcriptional programs. Results Using micrococcal nuclease treatment and high-throughput sequencing, we map genome-wide changes in nucleosome positioning in primary human endothelial cells stimulated with tumour necrosis factor alpha (TNFalpha) - a proinflammatory cytokine that signals through nuclear factor kappaB (NF-kappaB). Within 10 minutes, nucleosomes reposition at regions both proximal and distal to NF-kappaB binding sites, before the transcription factor quantitatively binds thereon. Similarly, in long TNFalpha-responsive genes, repositioning precedes transcription by pioneering elongating polymerases and appears to nucleate from intragenic enhancer clusters resembling super-enhancers. By 30 minutes, widespread repositioning occurs throughout Mbp-long chromosomal segments, with consequential effects on 3D structure, detected using chromosome conformation capture. Conclusions Whilst nucleosome repositioning is viewed as a local phenomenon, our results point to effects occurring over multiple scales. Here, we present data in support of a TNFalpha-induced priming mechanism, mostly independent of NF-kappaB binding and/or elongating RNA polymerases, leading to a plastic network of interactions that affects DNA accessibility over large domains. MNase-Seq of HUVEC cells after stimulation with TNFÎ± for 0, 10 or 30 min. Biological replicates for 0 and 30 min.

2014-11-05 | E-GEOD-53343 | biostudies-arrayexpress

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