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C-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program

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

ORGANISM(S): Mus musculus

PROVIDER: GSE137322 | GEO | 2019/09/13

REPOSITORIES: GEO

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c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program.

Project description:CCR6- group 3 innate lymphoid cells (ILC3s) are mediators of intestinal immunity and barrier function that possess the capacity to acquire type 1 effector features and fully convert into ILC1s. The molecular mechanisms governing such plasticity are undefined. Here, we identified c-Maf as an essential regulator of ILC3 homeostasis and plasticity that limits physiological ILC1 conversion. Phenotypic analysis of effector status in Maf-deficient CCR6- ILC3s, coupled with evaluation of global changes in transcriptome, chromatin accessibility, and transcription factor motif enrichment, revealed that c-Maf enforces ILC3 identity. c-Maf promoted ILC3 accessibility and supported ROR?t activity and expression of type 3 effector genes. Conversely, c-Maf antagonized type 1 programming, largely through restraint of T-bet expression and function. Mapping of the dynamic changes in chromatin landscape accompanying CCR6- ILC3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type 1 regulatory transformation and a controller of ILC3 fate.

| S-EPMC7037249 | biostudies-literature

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [RNA-seq]

Project description:The transcription factor c-Maf is an essential regulator of group 3 ILC homeostasis and effector plasticity. c-Maf limits acquisition of the type 1 program and conversion to the ILC1 fate through restraint of T-bet expression and function.

2019-09-13 | GSE137321 | GEO

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [CUT&RUN]

2019-09-13 | GSE137320 | GEO

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [ATAC-seq]

2019-09-13 | GSE137319 | GEO

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program

Project description:c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program

| PRJNA565163 | ENA

G9a regulates group 2 innate lymphoid cell development by repressing the group 3 innate lymphoid cell program.

Project description:Innate lymphoid cells (ILCs) are emerging as important regulators of homeostatic and disease-associated immune processes. Despite recent advances in defining the molecular pathways that control development and function of ILCs, the epigenetic mechanisms that regulate ILC biology are unknown. Here, we identify a role for the lysine methyltransferase G9a in regulating ILC2 development and function. Mice with a hematopoietic cell-specific deletion of G9a (Vav.G9a(-/-) mice) have a severe reduction in ILC2s in peripheral sites, associated with impaired development of immature ILC2s in the bone marrow. Accordingly, Vav.G9a(-/-) mice are resistant to the development of allergic lung inflammation. G9a-dependent dimethylation of histone 3 lysine 9 (H3K9me2) is a repressive histone mark that is associated with gene silencing. Genome-wide expression analysis demonstrated that the absence of G9a led to increased expression of ILC3-associated genes in developing ILC2 populations. Further, we found high levels of G9a-dependent H3K9me2 at ILC3-specific genetic loci, demonstrating that G9a-mediated repression of ILC3-associated genes is critical for the optimal development of ILC2s. Together, these results provide the first identification of an epigenetic regulatory mechanism in ILC development and function.

| S-EPMC4925019 | biostudies-literature

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [RNA-seq]

Project description:c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [RNA-seq]

| PRJNA565166 | ENA

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [ATAC-seq]

Project description:c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [ATAC-seq]

| PRJNA565165 | ENA

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [CUT&RUN]

Project description:c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [CUT&RUN]

| PRJNA565167 | ENA

c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells.

Project description:RORγt+ group 3 innate lymphoid cells (ILC3s) maintain intestinal homeostasis through secretion of type 3 cytokines such as interleukin (IL)-17 and IL-22. However, CCR6- ILC3s additionally co-express T-bet allowing for the acquisition of type 1 effector functions. While T-bet controls the type 1 programming of ILC3s, the molecular mechanisms governing T-bet are undefined. Here, we identify c-Maf as a crucial negative regulator of murine T-bet+ CCR6- ILC3s. Phenotypic and transcriptomic profiling of c-Maf-deficient CCR6- ILC3s revealed a hyper type 1 differentiation status, characterized by overexpression of ILC1/NK cell-related genes and downregulation of type 3 signature genes. On the molecular level, c-Maf directly restrained T-bet expression. Conversely, c-Maf expression was dependent on T-bet and regulated by IL-1β, IL-18 and Notch signals. Thus, we define c-Maf as a crucial cell-intrinsic brake in the type 1 effector acquisition which forms a negative feedback loop with T-bet to preserve the identity of CCR6- ILC3s.

| S-EPMC7025824 | biostudies-literature

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