Expression profiling of terminal B cell differentiation [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564229 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10077582.fastq.gz | Fastqsanger.gz | |||
| SRR10077583.fastq.gz | Fastqsanger.gz | |||
| SRR10077584.fastq.gz | Fastqsanger.gz | |||
| SRR10077585.fastq.gz | Fastqsanger.gz | |||
| SRR10077586.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin accessibility profiling of terminal B cell differentiation [ATAC-Seq]
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Project description:The terminal differentiation of B cells into antibody-secreting cells (ASCs) is a critical component of adaptive immune responses. Using our in vitro differentiation system, we combined RNA sequencing with ATAC-seq to characterize genomic events driving the ASC differentiation of human primary naive B cells. After an initial response to IL-4, cells that committed to an ASC fate downregulated the CD23 marker and IL-4 signaling, whereas cells that maintained IL-4 signaling did not differentiate. As demonstrated in the mouse, downregulation of the human ubiquitin ligase CBLB was required to free IRF4 from proteasomal degradation and produce levels needed for ASC differentiation. Our results evidenced two previously undocumented mechanisms driving human terminal B cell differentiation. Lastly, we showed that CD23-negative cells (i) carried the imprint of their previous activated B-cell status, (ii) were precursors of plasmablasts, and (iii) had a similar phenotype to in vivo pre-plasmablasts.
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Project description:Transcriptional profiling of Ampk-deficient B cells during terminal differentiation
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Project description:The terminal differentiation of B cells into antibody-secreting cells (ASCs) is a critical component of adaptive immune responses. Using our in vitro differentiation system, we combined RNA sequencing with ATAC-seq to characterize genomic events driving the ASC differentiation of human primary naive B cells. After an initial response to IL-4, cells that committed to an ASC fate downregulated the CD23 marker and IL-4 signaling, whereas cells that maintained IL-4 signaling did not differentiate. As demonstrated in the mouse, downregulation of the human ubiquitin ligase CBLB was required to free IRF4 from proteasomal degradation and produce levels needed for ASC differentiation. Our results evidenced two previously undocumented mechanisms driving human terminal B cell differentiation. Lastly, we showed that CD23-negative cells (i) carried the imprint of their previous activated B-cell status, (ii) were precursors of plasmablasts, and (iii) had a similar phenotype to in vivo pre-plasmablasts.
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Project description:Primary murine fetal liver cells were freshly isolated from day e14.5 livers and then sorted for successive differentiation stages by Ter119 and CD71 surface expression (ranging from double-negative CFU-Es to Ter-119 positive enucleated erythrocytes) [Zhang, et al. Blood. 2003 Dec 1; 102(12):3938-46]. RNA isolated from each freshly isolated, stage-sorted population was reverse-transcribed, labelled, and then hybridized onto 3' oligo Affymetrix arrays. Important erythroid specific genes as well as the proteins that regulate them were elucidated through this profiling based on coexpression and differential expression patterns as well as by extracting specific GO categories of genes (such as DNA-binding proteins). Abstract (submitted paper): rationale for expression profiling Gene-targeting experiments report that the homeodomain-interacting protein kinases 1 and 2, Hipk1 and Hipk2, are essential but redundant in hematopoietic developmentâbecause Hipk1/Hipk2 double-deficient animals exhibit severe defects in hematopoiesis and vasculogenesis while the single knockouts do not. These serine-threonine kinases phosphorylate, and consequently modify the functions of, several important hematopoietic transcription factors and cofactors. Here we show that Hipk2 knockdown alone plays a significant role in terminal fetal liver erythroid differentiation. Hipk1 and Hipk2 are highly induced during primary mouse fetal liver erythropoiesis. Specific knockdown of Hipk2 inhibits terminal erythroid cell proliferationâexplained in part by impaired cell cycle progression as well as increased apoptosisâand terminal enucleation as well as the accumulation of hemoglobin. Hipk2 knockdown also reduces the transcription of many genes involved in proliferation and apoptosis as well as important, erythroid-specific genes involved in hemoglobin biosynthesisâsuch as alpha-globin and mitoferrin 1âdemonstrating that Hipk2 plays an important role in some but not all aspects of normal terminal erythroid differentiation.
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Project description:Studying the function of common genetic variants in primary human tissues and during development is challenging. To address this, we use an efficient multiplexing strategy to differentiate 215 human induced pluripotent stem cell (iPSC) lines toward a midbrain neural fate, including dopaminergic neurons, and use single-cell RNA sequencing (scRNA-seq) to profile over 1 million cells across three differentiation time points. The proportion of neurons produced by each cell line is highly reproducible and is predictable by robust molecular markers expressed in pluripotent cells. Expression quantitative trait loci (eQTL) were characterized at different stages of neuronal development and in response to rotenone-induced oxidative stress. Of these, 1,284 eQTL colocalize with known neurological trait risk loci, and 46% are not found in the Genotype-Tissue Expression (GTEx) catalog. Our study illustrates how coupling scRNA-seq with long-term iPSC differentiation enables mechanistic studies of human trait-associated genetic variants in otherwise inaccessible cell states.
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Project description:Tet3 regulates terminal cell differentiation at the metabolic level
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Project description:Many postmitotic tissues coordinate robust cell cycle exit with the progression of terminal differentiation. While the signals involved in initiating cell cycle exit during terminal differentiation for some tissues have been described, less is known about the mechanisms that maintain a stable, non-cycling state. We previously found that chromatin accessibility changes at a subset of rate-limiting cell cycle genes occurs during maintenance of cell cycle exit, suggesting chromatin remodelers may play a key role in maintaining a robust postmitotic state during terminal differentiation. Here we show that the chromatin remodeler Mi-2 is required to ensure a stable, postmitotic state in Drosophila eyes and wings. Mi-2 alters chromatin accessibility and gene expression during cell cycle exit and terminal differentiation. Mi-2 and a transcription factor involved in tissue maturation, E93, close chromatin accessibility at an overlapping subset of potential enhancers that include the rate-limiting mitotic regulator string (cdc25c) and genes involved in the progression of terminal differentiation. E93 is also required for a stable, postmitotic state and we verified in vivo that Mi-2 and E93 cooperate to decommission an enhancer for the essential mitotic regulator string, to coordinate the transition to a postmitotic state with terminal differentiation. Enhancer decommissioning at the string locus provides a molecular explanation for the long-term, nearly irreversible postmitotic state observed in many tissues as terminal differentiation progresses.
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