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The transcription factor BCL6 controls early development of innate-like T cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE134212 | GEO | 2020/07/27

REPOSITORIES: GEO

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The transcription factor BCL6 controls early development of innate-like T cells (ATAC-seq)

Project description:Innate T cells, including invariant natural killer T (iNKT) and mucosal-associated innate T (MAIT) cells, are a heterogeneous T lymphocyte population with effector properties pre-programmed during their thymic differentiation. How this program is initiated is currently unclear. Here, we show that the transcription factor BCL6 is transiently expressed in iNKT cells upon exit from positive selection and is required for their proper development beyond stage 0. Notably, development of MAIT cells is also impaired in Bcl6-deficient mice. We found that BCL6 regulates the expression of genes that are associated with the innate T cell lineage, including PLZF and its targets. BCL6 contributes to a chromatin accessibility landscape that is permissive for the expression of development-related genes and inhibitory for genes associated with naïve T cell programs. Our results reveal novel functions for BCL6 and indicate that this transcription factor controls the inception of innate T cell lineage programming.

2020-07-27 | GSE134210 | GEO

The transcription factor BCL6 controls early development of innate-like T cells (RNA-seq)

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The transcription factor BCL-6 controls early development of innate-like T cells.

Project description:Innate T cells, including invariant natural killer T (iNKT) and mucosal-associated innate T (MAIT) cells, are a heterogeneous T lymphocyte population with effector properties preprogrammed during their thymic differentiation. How this program is initiated is currently unclear. Here, we show that the transcription factor BCL-6 was transiently expressed in iNKT cells upon exit from positive selection and was required for their proper development beyond stage 0. Notably, development of MAIT cells was also impaired in the absence of Bcl6. BCL-6-deficient iNKT cells had reduced expression of genes that were associated with the innate T cell lineage, including Zbtb16, which encodes PLZF, and PLZF-targeted genes. BCL-6 contributed to a chromatin accessibility landscape that was permissive for the expression of development-related genes and inhibitory for genes associated with naive T cell programs. Our results revealed new functions for BCL-6 and illuminated how this transcription factor controls early iNKT cell development.

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Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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The transcription factor BCL6 controls early development of innate-like T cells

Project description:The transcription factor BCL6 controls early development of innate-like T cells

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Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

Project description:This SuperSeries is composed of the SubSeries listed below.

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BCL6 controls Th9 cell development by repressing Il9 transcription.

Project description:The transcriptional repressor B cell lymphoma 6 (BCL6) is required for the development of Th follicular cells, and it has been shown to suppress Th2 cell differentiation. We demonstrate that BCL6 is a key regulator of Th9 cell development. BCL6 expression is transiently downregulated in polarized Th9 cells, and forced expression of BCL6 in Th9 cells impairs Th9 cell differentiation. In contrast, BCL6 knockdown upregulated IL-9 production in Th9 cells. The function of BCL6 in Th9 cells is under the control of IL-2/JAK3/STAT5 signaling pathway. Using chromatin immunoprecipitation, we show that, in Th9 cells, BCL6 and STAT5 bind to adjacent motifs in the Il9 promoter. Furthermore, we found that STAT5 binding was associated with the abundance of a permissive histone mark at the Il9 promoter, whereas under conditions in which BCL6 binding was predominant, a repressive histone mark was prevalent. The effects of STAT5 and BCL6 on IL-9 transcription were further demonstrated using an IL-9 luciferase reporter assay in which BCL6 repressed STAT5-mediated Il9 transactivation. In experimental autoimmune encephalomyelitis, forced expression of BCL6 in myelin oligodendrocyte glycoprotein35-55-specific Th9 cells resulted in decreased IL-9 production and induction of IFN-γ, causing an exacerbation of the clinical disease. Our findings demonstrate a novel role of BCL6 in the regulation of Th9 cell development and their encephalitogenicity.

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Global translation during early development depends on the essential transcription factor PRDM10

Project description:This SuperSeries is composed of the SubSeries listed below.

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Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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