Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1149536 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30293671.fastq.gz | Fastqsanger.gz |
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Project description:T cell precursors develop into cytotoxic CD8 and helper CD4+ T cells in thymus. Thpok, a BTB/POZ family transcription factor, enforces commitment to the CD4 lineage and suppresses cytotoxic gene expression. However, it is still not fully understood how Thpok directs CD4 T cell development. Here, using mass-spectrometry, we identify nucleosome remodeling and deacetylase (NuRD) complex as a novel Thpok cofactor. We demonstrate that the Thpok BTB domain is essential for NuRD recruitment. Reconstituting NuRD binding to a BTB-less version of Thpok (which cannot bind NuRD) restored CD4 T cell in vivo. RNA sequencing showed that CD4 T cells expressing the reconstituted protein express a transcriptome similar to that of CD4 T cells expressing Thpok. Thus, our results demonstrate that NuRD recruitment is both necessary and sufficient for the function of the Thpok BTB domain in CD4 T cell development.
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Project description:ZBTB4 is a mammalian transcription factor with Zinc fingers and a BTB/POZ domain, which can bind methylated CpGs, as well as certain unmethylated consensus sequences. ZBTB4 is frequently downregulated in human cancers, but it is unclear whether this is a cause or consequence of transformation. To investigate the role of ZBTB4 in normal and pathological conditions, we generated Zbtb4-/- mice
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Project description:Mice: knock-out of the Miz1 POZ-domain in brain (Miz1DPOZNes) and control mice. The RNA expression in cerebella of of old Miz1 delta POZ mice (1.5 years), old control mice (1.5 years), young Miz1 delta POZ mice (5.5 weeks) and young control mice (5.5 weeks) was compared
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Project description:The transcription factor Bcl6 orchestrates the germinal center reaction through its actions in B and T cells, and regulates inflammatory signaling in macrophages. We report that genetic replacement by mutant Bcl6, which cannot bind corepressors to its BTB domain, disrupted  germinal center formation and immunoglobulin affinity maturation, due to a defect in B cell  proliferation and survival. In contrast, BTB loss of function had no effect on T follicular helper cell differentiation and function, nor other T helper subsets. Bcl6 null mice displayed a lethal inflammatory phenotype, whereas BTB mutant mice experienced normal healthy lives with no inflammation. Bcl6 repression of inflammatory responses in macrophages was accordingly independent of the BTB domain repressor function. Bcl6 thus mediates its actions through lineage-specific biochemical functions. ChIP-seq for Bcl6, SMRT and BCOR in germinal center B cells
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Project description:Although BTB-zinc finger (BTB-ZF) transcription factors control the differentiation of multiple hematopoietic and immune lineages, how they function is poorly understood. The BTB-ZF factor Thpok controls intrathymic CD4+ T cell development and expression of most CD4+- and CD8+-lineage genes. Here, we identify the nucleosome remodeling and deacetylase (NuRD) complex as a novel Thpok cofactor. We locate three amino-acid residues within the Thpok BTB domain that are required for both NuRD binding and Thpok functions, and show that NuRD recruitment recapitulates the functions of the Thpok BTB domain. NuRD mediates Thpok repression of CD8+-lineage genes, including the transcription factor Runx3, but is dispensable for Cd4 expression. We show that these functions cannot be performed by the BTB domain of the Thpok-related factor Bcl6, which fails to bind NuRD. Thus, cofactor binding critically contributes to the functional specificity of BTB-zinc finger factors, which control the differentiation of most hematopoietic subsets.
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Project description:T cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease mainly affecting children. Relapse rates are high and toxic chemotherapies that block DNA replication and induce DNA damage cause health problems later in life, underlining the need for improved therapies. We show that ablation of the BTB/POZ domain factor Miz-1 significantly delays Notch1-induced T-ALL in mice through induction of p53-dependent cell death. Leukemic cells that still emerge in this system activate DNA replication and strand elongation pathways, which are those targeted by current chemotherapeutic drugs such as cytarabine. Acute Miz-1 ablation enhances the effect of cytarabine treatment and eliminates leukemic cells completely in some cases, suggesting that targeting Miz-1 could render current T-ALL chemotherapies more effective.
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