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The subtype-specific transcriptional regulatory networks of intestinal innate lymphoid cells

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

ORGANISM(S): Mus musculus

PROVIDER: GSE116093 | GEO | 2019/05/21

REPOSITORIES: GEO

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The subtype-specific transcriptional regulatory networks of intestinal innate lymphoid cells (RNA-seq)

Project description:Innate lymphoid cells (ILCs) comprise a population of immune cells that promote tissue homeostasis, defense against infections, and inflammatory disease. Yet, the transcriptional control of these functions is not well understood. Here, we leverage an experimental-computational approach for transcriptional regulatory network (TRN) inference, recently validated in an in vitro context, to construct genome-scale TRNs for ILCs isolated ex vivo from the intestine of mice. Chromatin accessibility and gene expression are the key data for our TRN inference method. Thus, we generated ATAC-seq and RNA-seq datasets for ILCs of the small and large intestine to integrate with publicly available ILC genomics data. From our ILC TRN, we predict target genes for hundreds of transcription factors (TFs), recovering both known and novel TF regulators of ILC subtype-specific gene expression patterns. The identified TFs include both activators and repressors of lineage-specific genes. Using KO mice, we validated predictions for two such TFs, MAF and BCL6, as previously unknown regulators affecting the balance of ILC3-ILC1. We additionally demonstrate the utility of our ILC TRN to describe gene expression responses to Bcl6 KO in ILC1, NK and ILC3 and predict TF regulators in each subtype. The ILC TRN and “core” ILC subtype networks are publicly available through an interactive Jupyter-notebook web interface. We anticipate that these maps of ILC subtype-specific transcriptional regulation will serve as an important community resource and lead to the development of new strategies for the control of subtype-specific behaviors, especially in the context of disease.

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

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Project description:Innate lymphoid cells (ILCs) promote tissue homeostasis and immune defense but also contribute to inflammatory diseases. ILCs exhibit phenotypic and functional plasticity in response to environmental stimuli, yet the transcriptional regulatory networks (TRNs) that control ILC function are largely unknown. Here, we integrate gene expression and chromatin accessibility data to infer regulatory interactions between transcription factors (TFs) and genes within intestinal type 1, 2, and 3 ILC subsets. We predicted the "core" TFs driving ILC identities, organized TFs into cooperative modules controlling distinct gene programs, and validated roles for c-MAF and BCL6 as regulators affecting type 1 and type 3 ILC lineages. The ILC network revealed alternative-lineage-gene repression, a mechanism that may contribute to reported plasticity between ILC subsets. By connecting TFs to genes, the TRNs suggest means to selectively regulate ILC effector functions, while our network approach is broadly applicable to identifying regulators in other in vivo cell populations.

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The subtype-specific transcriptional regulatory networks of intestinal innate lymphoid cells (ATAC-seq)

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Project description:The discovery of the specification of CD4(+) helper T cells to discrete effector 'lineages' represented a watershed event in conceptualizing mechanisms of host defense and immunoregulation. However, our appreciation for the actual complexity of helper T-cell subsets continues unabated. Just as the Sami language of Scandinavia has 1000 different words for reindeer, immunologists recognize the range of fates available for a CD4(+) T cell is numerous and may be underestimated. Added to the crowded scene for helper T-cell subsets is the continuously growing family of innate lymphoid cells (ILCs), endowed with common effector responses and the previously defined 'master regulators' for CD4(+) helper T-cell subsets are also shared by ILC subsets. Within the context of this extraordinary complexity are concomitant advances in the understanding of transcriptomes and epigenomes. So what do terms like 'lineage commitment' and helper T-cell 'specification' mean in the early 21st century? How do we put all of this together in a coherent conceptual framework? It would be arrogant to assume that we have a sophisticated enough understanding to seriously answer these questions. Instead, we review the current status of the flexibility of helper T-cell responses in relation to their genetic regulatory networks and epigenetic landscapes. Recent data have provided major surprises as to what master regulators can or cannot do, how they interact with other transcription factors and impact global genome-wide changes, and how all these factors come together to influence helper cell function.

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