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Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by enzymatic-methyl sequencing

ABSTRACT: We are interested in deciphering the mechanism by which DNA methylation in late B cell differentiation affects humoral immune response. We were using enzymatic-methyl sequencing (EM-seq) and chose to study a very rare immunodeficiency called ICF type 4, where a point mutation in a gene encoding the protein HELLS causes a lack of both circulating antibodies and memory B cells in human. HELLS is a chromatin remodeler, that allows for DNA methylation to occur.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Charles Girardot

PROVIDER: E-MTAB-12609 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by single-cell RNA sequencing

Project description:We are interested in deciphering the mechanism by which DNA methylation in late B cell differentiation affects humoral immune response. We chose to study a very rare immunodeficiency called ICF type 4, where a point mutation in a gene encoding the protein HELLS causes a lack of both circulating antibodies and memory B cells in human. HELLS is a chromatin remodeler, that allows for DNA methylation to occur. Using a Hells conditional knock-out in B cells, we measured the kinetics of the immune B cell response, following immunization with NP-CGG, and show a lack of memory and plasma cells accompanied by a defect in germinal center maintenance, but not by its formation. Single cell RNAseq of cell sorted naive, germinal center B cells and memory B cells at day 7 and day 14 post NP-immunization helped us better characterize the phenotype.

2023-07-25 | E-MTAB-12499 | biostudies-arrayexpress

Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by bulk RNA sequencing.

Project description:The transcriptomic impact of Hells loss-of-function was quantified by RNA sequencing of sample from conditional knockout (Mb1-Cre+/WT HellsF/F) and littermate control mice (Mb1-CreWT/WT HellsF/F). Three time points were chosen to follow the kinetic: day 0 for naïve B cells collection, day 7 and day 14 post NP-CGG intraperitoneal immunization for germinal center B cells collection. At each time point, 4 mice of each genotype were used. Live cells were FACS sorted (AriaIII) using surface markers as follows: B220+CD21+CD23+ for naïve B cells, and B220+CD95+GL7+ for germinal center B cells. Due to their low frequency, germinal center B cells were FACS-sorted twice using the same gating strategy. Collected samples were lysed and processed for RNA extraction.

2023-07-25 | E-MTAB-12638 | biostudies-arrayexpress

Murine germinal center and naive B cells

Project description:Gene expressions of murine germinal center and naive B cells on Affymetrix platform The experiment include 3 d14 GC B1-8, 3 d14 GC V23 and 4 NaM-CM-/ve samples

2013-03-06 | E-GEOD-44260 | biostudies-arrayexpress

T cell dependent immune responses: B cell activation and differentiation Group1 Fo, Group2 GC1, Group3 GC2

Project description:Upon immunization with a T cell dependent antigen naive follicular B cells (Fo) are activated and a germinal center reaction is induced. Within the next 2 weeks large germinal centers develop where the process of affinity maturation takes place. To analyze the gene expression profile of resting and activated B cells, follicular B cells (Fo), B cells from early (GC1) and late germinal centers (GC2) were isolated and their gene expression profile compared. Gene expression profiles of Fo versus GC1 and GC2 B cells, respectively. Naïve Fo B cells were isolated from non-immunized BALB/c mice. Germinal center B cells sorted from spleen cell suspensions of BALB/-c mice immunized with the T cell dependent antigen 2-phenyl Oxazolone. GC1 B cells were isolated 7 days after primary immunization. GC2 cells were isolated 15 days after primary immunization. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 µg cRNA hybridized in duplicates for each of the three groups to the GeneChip arrays. Group1: Fo, Group2: GC1, Group3: GC2. Lists of differentially regulated genes were created using High Performance Chip Data Analysis (HPCDA) with Bioretis database (http://www.bioretis-analysis.de). Worldwide data sharing is possible via Bioretis, please ask the authors.

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The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

Project description:The activating E2F-transcription factors are best known for their dependence on the Retinoblastoma protein and their role in cellular proliferation. E2F3 is uniquely amplified in specific human tumours where its expression is inversely correlated with the survival of patients. Here, E2F3 interaction partners were identified by mass spectrometric analysis. We show that the SNF2-like HELLS interacts with E2F3 in vivo and cooperates with its oncogenic functions. Depletion of HELLS severely perturbs the induction of E2F-target genes, hinders cell cycle re-entry and growth. Using chromatin immmunoprecipitation coupled to sequencing we identified genome-wide targets of HELLS and E2F3. Our analysis revealed that HELLS binds near promoters of active genes, including the trithorax-related MLL1, and co-regulates E2F3-dependent genes. Our analysis is the first to link HELLS with E2F-controlled processes that are critical to establish a proliferative tumour circuitry. Strikingly, just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours. Our work reveals that HELLS is important for E2F3 in tumour cell proliferation. Examination of E2F3, Hells, and H3K27me3 in 2 cell types.

2011-12-19 | E-GEOD-33791 | biostudies-arrayexpress

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

2011-12-19 | GSE33791 | GEO

ChIP-seq of human ALK negative ALCL cell line (TLBR2) in parental and HELLS knockdown conditions

Project description:Characterization of transcriptional landscape of HELLS in T-cell lymphoma. ChIP-seq experiments against Histone Marks and RNA-Polymerase II were performed in both control and HELLS knockdown (DOX) cells. ChIP-seq against HELLS was performed in control cells.

2024-06-06 | E-MTAB-12935 | biostudies-arrayexpress

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Tumors from Rb1/p107 DKO and Rb1/p107/Hells TKO mice were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE143732 | GEO

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Retinae from Rb1/p107 DKO and Rb1/p107/Hells TKO mice at postnatal day 21 were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE144427 | GEO

PRDM9 activity depends on HELLS and promotes 5-Hydroxymethylcytosine enrichment

Project description:Meiotic recombination starts with the formation of DNA double-strand breaks (DSBs) at specific genomic locations that correspond to PRDM9-binding sites. The molecular steps occurring from PRDM9 binding to DSB formation are unknown. Using proteomic approaches to find PRDM9 partners, we identified HELLS, a member of the SNF2-like family of chromatin remodelers. Upon functional analyses during mouse male meiosis, we demonstrated that HELLS is required for PRDM9 binding and DSB activity at PRDM9 sites. However, HELLS is not required for DSB activity at PRDM9-independent sites. HELLS is also essential for 5-hydroxymethylcytosine (5hmC) enrichment at PRDM9 sites. Analyses of 5hmC in mice deficient for SPO11, which catalyzes DSB formation, and in PRDM9 methyltransferase deficient mice reveal that 5hmC is triggered at DSB-prone sites upon PRDM9 binding and histone modification, but independent of DSB activity. These findings highlight the complex regulation of the chromatin and epigenetic environments at PRDM9-specified hotspots.

2020-11-19 | GSE145768 | GEO

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