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HDAC1 and 2 repress lineage inappropriate expression of Flt3 and Ptprf in B cells via Pax5 and Grg4

ABSTRACT: Total RNA was isolated from pre BI (early lymphcytes) cells sorted by FACS with the following markers: B220+, CD25-, C-kit+,IgM-, CD19+. The animals used carried floxed Hdac1 & 2 either in combination with mb1-cre (refered to as DKO) or not (WT).

ORGANISM(S): Mus musculus

PROVIDER: GSE36564 | GEO | 2016/03/16

SECONDARY ACCESSION(S): PRJNA153717

REPOSITORIES: GEO

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HDAC1 and 2 repress lineage inappropriate expression of Flt3 and Ptprf in B cells via Pax5 and Grg4

Project description:Total RNA was isolated from pre BI (early lymphcytes) cells sorted by FACS with the following markers: B220+, CD25-, C-kit+,IgM-, CD19+. The animals used carried floxed Hdac1 & 2 either in combination with mb1-cre (refered to as DKO) or not (WT). 6 samples of FACS-sorted pre BI cells were analyzed, corresponding to 6 individual female animals, 8 week of age, 3 per genotype DKO and WT.

2016-03-16 | E-GEOD-36564 | biostudies-arrayexpress

HDAC1 Frameshiftting IP mass spectrometry

Project description:In eukaryotes, several gene have been found that ribosomal frameshifting efficiently occurs on its slippery site. However, less study focuses on codon repeat induce frameshifting. To screen whether the codon repeat in HDAC1 gene could induced frameshifting and produce frameshifting peptide. we generate a HDAC1-FS-Flag construct. Detection the HDAC1 frameshifting protein using immunoprecipitation-Mass Spectrometry.

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Zebrafish hdac1 mutant and morphant embryos

Project description:This SuperSeries is composed of the following subset Series: GSE26707: Zebrafish 27hpf embryos: hdac1 mutant (hi1618) vs sibling GSE26708: Zebrafish embryos: hdac1 Morphants vs Standard control morphants GSE26709: Zebrafish embryos: hdac1 Morphants vs Standard control morphants at 12, 18 and 27 hpf Refer to individual Series

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Zebrafish embryos: hdac1 Morphants vs Standard control morphants

Project description:Transcriptional profiling of hdac1 morphant zebrafish embryos in comparison to standard control injected embryos. Embryos where injected at the one cell stage with either a translation blocking morpholino (Hdac1 ATG), splice blocking morpholino (Hdac1 Splice) or Hdac1 mismatch control morpholino (Hdac1 control). RNA was extracted and compared in a two-colour hybridisation to the comman reference Standard control morpholino injected embryos. Common reference experiment, hdac1 morphants vs. standard control morphants. Biological replicates: 2 (except Splice which was technical rather than biological)

2011-01-21 | E-GEOD-26708 | biostudies-arrayexpress

GSE1 is a prominent interactor of HDAC1

Project description:We analysed the composition of histone acetylase 1 (HDAC1)-associated proteins in different cellular backgrounds using quantitative mass spectrometry (MS). First, we affinity purified (AP) C-terminally FLAG-tagged HDAC1 from the nearly haploid human cell line HAP1 (Andersson et al, 1987). To examine cross-species conservation in the composition of HDAC1 complexes we additionally analysed HDAC1-FLAG purifications from mouse embryonic fibroblasts (MEFs). Genetic suppressor element 1 (GSE1) was identified as a prominent interaction partner of HDAC1. Hence, we purified V5-tagged GSE1 from HAP1 cells and analysed co-precipitated proteins.

2023-10-23 | PXD040307 | Pride

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.

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HDAC1/2 and CD4+ T cells

Project description:Dynamic changes in histone acetylation patterns are mediated by the activity of histone acetyltransfereases (HATs) and histone deacetylases (HDACs) and are key events in the epigenetic regulation of gene expression. The application of HDAC inhibitors revealed a variety of T cell functions controlled by reversible lysine acetylation and HDAC1, HDAC2, HDAC3, HDAC7 and HDAC9 have been implicated in regulating T cell development and function. Nevertheless, unique functions of individual HDAC members in T cells and specific T cell functions that are regulated by HDACs are still only poorly understood. We previously showed that T cell-specific loss of HDAC1 (using the Cd4Cre deleter strain) leads to enhanced allergic airway inflammation and increased Th2 cytokine production. Interestingly, late T cell development was not impaired in these mice. However, HDAC2 was up-regulated in the absence of HDAC1, thus we hypothesized compensatory pathways/function between these two closely related class I HDAC family members in T cells. To investigate redundant and non-redundant functions of HDAC1 and HDAC2, we generated mice with a conditional T cell-specific (using Cd4Cre) combined loss of HDAC1 and HDAC2. As part of our study, we determined and compared the transcriptome of peripheral wild-type and HDAC1/2-null CD4+ T cells. Since loss of HDAC1/HDAC2 during late T cell development led to the appearance of MHC class II-selected CD4+ helper T cells that expressed CD8 lineage genes such as Cd8a and Cd8b1, we also analyzed the transcriptome of HDAC1/2-null CD4+CD8+ T cells.

2014-03-30 | E-MTAB-2184 | biostudies-arrayexpress

Functional Roles of Hdac1/2 in lung development

Project description:Hdac1/2 are important epigenetic factors, yet their functional roles in specific tissues inluding lung is not determined. We used the conditional knockout model of Hdac1/2 to determine their roles in lung development. To explore the genes that are regulated by Hdac1/2 during lung development, we performed microarray analysis of Shhcre control and Hdac1/2DKO lungs at E11.5 embryos.

2013-12-31 | E-GEOD-39946 | biostudies-arrayexpress

Transcriptome Analysis of IL-33-Deficient Early Developing B Cells

Project description:We identified that IL-33 is expressed in pro-B (B220+ IgM- CD19+ CD43+) and large pre-B cells (B220+ IgM- CD19+ CD43- FSC-Ahi SSC-Ahi) in mice. We assessed for IL-33-dependent gene expression differences in these B cell stages by performing bulk RNA-sequencing of FACS-purified pro-B and large pre-B cells from WT and IL-33-deficient 8 week old adult, naive female mice.

2019-07-04 | GSE132123 | GEO

Bi-phenotypic B-lymphoid/myeloid cells expressing low levels of Pax5 - potential targets of BAL development

Project description:Retroviral transduction of Pax5-deficient pro/preB cell lines with a doxycycline-inducible (TetON) form of the human Pax5 (huPax5) gene yielded cell clones which could be induced to different levels of huPax5 expression. Clones inducible to high levels developed B220+/CD19/+IgM+ B cells, while clones with low levels differentiated to B220+/CD19- /CD11b+/Gr-1- B-lymphoid/myeloid “bi-phenotypic” cells in vitro and in vivo. “Bi-phenotypic” cells could also be developed from high level-inducible cells by lower concentrations of doxycycline, inducing lower levels of huPax5 in vitro. Microarray analyses of genes expressed at these lower levels of huPax5 identified C/ebpα, C/ebpδ, Pu.1, Csf1r, Csf2r and Gata-3 as myeloid-related genes selectively expressed in the pro/preB cells which can develop under myeloid/lymphoid conditions to “bi-phenotypic” cells. Therefore, reduced expression of huPax5 during the induction of early lymphoid progenitors to B-lineage-committed cells can fix this cellular development at a stage that has previously been seen during embryonic development and in ALL-like “bi-phenotypic” acute leukemias (BAL).

2012-08-14 | GSE33875 | GEO

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