Distinct SWI/SNF chromatin remodelling complexes act differentially to maintain stem-like exhausted CD8 T cells [RNA-seq]
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PROVIDER: PRJNA870148 | ENA |
REPOSITORIES: ENA
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Project description:Distinct SWI/SNF chromatin remodelling complexes act differentially to maintain stem-like exhausted CD8 T cells.
| PRJNA870141 | ENA
Project description:Distinct SWI/SNF chromatin remodelling complexes act differentially to maintain stem-like exhausted CD8 T cells [ATAC-seq]
| PRJNA870147 | ENA
Project description:• Evolutionarily conserved SWI-SNF ATP-dependent chromatin remodeling complexes (CRCs) change nucleosome positioning and chromatin states, affecting gene expression to regulate important regulatory processes controlling such as proper development and hormonal signalling pathways. • In our study we used transcript profiling, chromatin immunoprecipitation (ChIP), exhaustive protein-protein interaction study including mass-spectrometry, yeast-two-hybrid and bimolecular fluorescence complementation (BiFC) along with hormone and metabolite profiling, and phenotype assessments to distinguish the functions of Arabidopsis SWP73A and SWP73B subunits in Arabidopsis. • We identified a novel subclass of SWI/SNF chromatin remodelling complexes defined by the presence of SWP73A subunit. Therefore, we propose a refined classification of SWI/SNF CRCs in Arabidopsis, introducing BAS-A (SWP73A-containing) and BAS-B (SWP73B-containing) subclasses. The SWP73A and SWP73B-carrying subclasses of SWI/SNF CRCs exhibit differential properties demonstrated by distinct chromatin binding patterns and divergent effect on hormone biosynthesis and metabolism. We found that SWP73A plays a specific role that cannot be fully compensated by SWP73B. We recognized that some atypical subclasses of SWI/SNF CRCs may be likely formed in mutant lines with inactivated SWP73 subunits. • Our study reveals that the duplication of the SWP73 subunit contributes to unique and shared functions of subclasses of SWI/SNF CRCs in the control of various regulatory processes in Arabidopsis.
2025-04-15 | PXD056187 | Pride
Project description:Exhausted CD8 T cells (TEX) arise during chronic viral infections and cancer and limit disease control. Three major sequential epigenetic remodeling events occur as naïve CD8 T cells (TN) differentiate into TEX: initial activation, early bifurcation between effector (TEFF) and TEX precursors, and later differentiation of effector-like and terminal TEX subsets from progenitor TEX. The epigenetic factors mediating these transitions remain poorly understood. Here, we uncovered distinct roles for two versions of the SWI/SNF chromatin remodeling complex, BAF and PBAF, in TEX differentiation using in vivo CRISPR screening. Disruption of BAF ablated antigen-specific CD8 T cells early in chronic infection, suggesting a requirement for BAF-mediated remodeling in the early epigenetic remodeling events. In contrast, depletion of PBAF subunits enhanced TEX formation and promoted progenitor TEX differentiation into more differentiated TEX subsets by limiting accessibility of TCF-1 binding sites. Loss of PBAF improved tumor control alone and in combination with anti-PD-L1. Simultaneous depletion of BAF- and PBAF-specific subunits revealed that BAF is required for the beneficial impact of loss of PBAF on TEX differentiation. Thus, BAF and PBAF regulate epigenetic transitions in CD8 T cell differentiation, with PBAF acting at a later stage in exhaustion as a guardian to limit full TEX differentiation and preserve TEX progenitor populations with implications for cancer immunotherapy.
2023-05-31 | GSE211410 | GEO
Project description:Exhausted CD8 T cells (TEX) arise during chronic viral infections and cancer and limit disease control. Three major sequential epigenetic remodeling events occur as naïve CD8 T cells (TN) differentiate into TEX: initial activation, early bifurcation between effector (TEFF) and TEX precursors, and later differentiation of effector-like and terminal TEX subsets from progenitor TEX. The epigenetic factors mediating these transitions remain poorly understood. Here, we uncovered distinct roles for two versions of the SWI/SNF chromatin remodeling complex, BAF and PBAF, in TEX differentiation using in vivo CRISPR screening. Disruption of BAF ablated antigen-specific CD8 T cells early in chronic infection, suggesting a requirement for BAF-mediated remodeling in the early epigenetic remodeling events. In contrast, depletion of PBAF subunits enhanced TEX formation and promoted progenitor TEX differentiation into more differentiated TEX subsets by limiting accessibility of TCF-1 binding sites. Loss of PBAF improved tumor control alone and in combination with anti-PD-L1. Simultaneous depletion of BAF- and PBAF-specific subunits revealed that BAF is required for the beneficial impact of loss of PBAF on TEX differentiation. Thus, BAF and PBAF regulate epigenetic transitions in CD8 T cell differentiation, with PBAF acting at a later stage in exhaustion as a guardian to limit full TEX differentiation and preserve TEX progenitor populations with implications for cancer immunotherapy.
2023-05-31 | GSE211409 | GEO
Project description:Evolutionary conserved SWI-SNF ATP-dependent chromatin remodeling complex changes nucleosome positioning and chromatin states, affecting gene expression to regulate developmental and hormonal pathways. We showed the SWP73A and SWP73B - subunits of the SWI/SNF complex - differentially regulate gene expression related to metabolism and hormone biosynthesis, with opposite chromatin occupancy profiles. The swp73b mutant exhibits hypersensitivity to auxin and salicylic acid (SA). SWP73B inactivation results in SA accumulation, but decreased gibberellin (GA) content and long-term GA treatment partially restored its phenotype. Both SWP73 subunits are required for maintaining proper diurnal metabolite profiles, with SWP73A regulating essential genes of raffinose and glucosinolate metabolism. Our study reveals that the duplication of the SWP73 subunit contributes to novel functions of the Arabidopsis SWI/SNF complex in gene transcription.
2025-04-10 | GSE261097 | GEO
Project description:BAF60/SWP73 Subunits Define Subclasses of SWI/SNF Chromatin Remodelling Complexes in Arabidopsis
| PRJNA1085280 | ENA
Project description:The 12-subunit Swi/Snf chromatin remodeling complex is conserved from yeast to humans. It functions to alter nucleosome positions by either sliding nucleosomes on DNA or evicting histones. Interestingly, 20% of all human cancers carry mutations in subunits of the Swi/Snf complex. Many of these mutations cause protein instability and loss, resulting in partial Swi/Snf complexes. Although several studies have shown that histone acetylation and activator-dependent recruitment of Swi/Snf regulate its function, it is less well understood how subunits regulate stability and function of the complex. Using functional proteomic and genomic approaches, we have assembled the network architecture of yeast Swi/Snf. In addition, we find that subunits of the Swi/Snf complex regulate occupancy of the catalytic subunit Snf2, thereby modulating gene transcription. Our findings have direct bearing on how cancer-causing mutations in orthologous subunits of human Swi/Snf may lead to aberrant regulation of gene expression by this complex.
2017-08-07 | MSV000081417 | MassIVE
Project description:The 12-subunit Swi/Snf chromatin remodeling complex is conserved from yeast to humans. It functions to alter nucleosome positions by either sliding nucleosomes on DNA or evicting histones. Interestingly, 20% of all human cancers carry mutations in subunits of the Swi/Snf complex. Many of these mutations cause protein instability and loss, resulting in partial Swi/Snf complexes. Although several studies have shown that histone acetylation and activator-dependent recruitment of Swi/Snf regulate its function, it is less well understood how subunits regulate stability and function of the complex. Using functional proteomic and genomic approaches, we have assembled the network architecture of yeast Swi/Snf. In addition, we find that subunits of the Swi/Snf complex regulate occupancy of the catalytic subunit Snf2, thereby modulating gene transcription. Our findings have direct bearing on how cancer-causing mutations in orthologous subunits of human Swi/Snf may lead to aberrant regulation of gene expression by this complex.
2017-08-07 | MSV000081418 | MassIVE
Project description:Loss of Swi/Snf subunits regulate transcription.
2017-02-17 | GSE81722 | GEO