Expression data from murine natural killer cell subsets based on Ly49 receptor expression in C57BL/6 mice (C/I+ versus Ly49G2+ NK cells)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE56662 | GEO | 2014/09/01
SECONDARY ACCESSION(S): PRJNA244240
REPOSITORIES: GEO
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Project description:Natural killer (NK) cells have differential expression of inhibitory and activating receptors. NK cells that express inhibitory receptors with high binding affinity to self are considered licensed and normally functional cells, while those with low affinity are unlicensed are considered hyporesponsive. Microarray analysis was performed to better understand gene expression differences between these two subpopulations of NK cells after culturing the NK cells with IL-2 from splenocytes isolated from C57BL/6 mice and then sorting for CD3-CD122+Ly49G2+Ly49C/I- or CD3-CD122+Ly49G2-Ly49C/I+. Gene fold expression differences were compared between the Ly49G2+ and Ly49C/I+ NK cells to better understand the functional roles and characterisitics of these cells. A total of 6 samples were analyzed, 3 for the CD3-CD122+Ly49G2+Ly49C/I- NK cells and 3 for the CD3-CD122+Ly49G2-Ly49C/I+. Samples were obtained from C57BL/5 splenocytes that were T cells depleted through anti-Thy1.2 and complement mediated depletion and cultured for 7 days with IL-2. Fold changes greater than 1.5 were recorded.
2014-09-01 | E-GEOD-56662 | biostudies-arrayexpress
Project description:Natural killer cells are cytotoxic lymphocytes important in immune responses to cancer and multiple pathogens. However, chronic activation of NK cells can induce a hyporesponsive state. The molecular basis of the mechanisms underlying the generation and maintenance of this hyporesponsive state are unknown, thus an easy and reproducible mechanism able to induce hyporesponsiveness on human NK cells would be very useful to gain understanding of this process. Human NK cells treated with ionomycin lose their ability to degranulate and secrete IFN-γ in response to a variety of stimuli, but IL-2 stimulation can compensate these defects. Apart from reductions in the expression of CD11a/CD18, no great changes were observed in the activating and inhibitory receptors expressed by these NK cells, however their transcriptional signature is different to that described for other hyporesponsive lymphocytes.
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Project description:Comparative genomics has revealed the rapid lineage-specific expansion of multiple gene families involved in immunity, presumably due to the complexity of ensuring pathogen defense while maintaining self-tolerance. Paralogs within these gene families often evolved distinct roles in immunity. However, less is known about how the epigenome and cis-regulation of these gene families evolved. Here we focus on the epigenetic evolution of the rapidly evolving murine Ly49 gene family. Ly49 genes mainly encode either inhibitory or activating surface receptors in natural killer (NK) cells. Together, they fine-tune NK cell activation. We systemically mapped Ly49 transcription initiation, chromatin accessibility, DNA methylation and 3D chromatin interactions. Our data revealed that each Ly49 gene forms a cis-regulatory unit consisted of one or more lowly accessible promoters and a proximal enhancer. Importantly, parallel to the functional divergence of the encoded proteins, inhibitory and activating Ly49 genes have evolved two separate sets of proximal enhancers, likely as a result of lineage-specific losses of enhancer activity. Finally, we show that some Ly49 genes can be cross-regulated by the enhancers of other Ly49 genes, suggesting that the Ly49 family have evolved a concerted regulatory mechanism. Collectively, we demonstrate the different modes of epigenetic evolution for a rapidly expanding gene family essential for host immunity, and provide a rich epigenetic dataset for NK cell research.
2024-04-20 | GSE226501 | GEO
Project description:Comparative genomics has revealed the rapid lineage-specific expansion of multiple gene families involved in immunity, presumably due to the complexity of ensuring pathogen defense while maintaining self-tolerance. Paralogs within these gene families often evolved distinct roles in immunity. However, less is known about how the epigenome and cis-regulation of these gene families evolved. Here we focus on the epigenetic evolution of the rapidly evolving murine Ly49 gene family. Ly49 genes mainly encode either inhibitory or activating surface receptors in natural killer (NK) cells. Together, they fine-tune NK cell activation. We systemically mapped Ly49 transcription initiation, chromatin accessibility, DNA methylation and 3D chromatin interactions. Our data revealed that each Ly49 gene forms a cis-regulatory unit consisted of one or more lowly accessible promoters and a proximal enhancer. Importantly, parallel to the functional divergence of the encoded proteins, inhibitory and activating Ly49 genes have evolved two separate sets of proximal enhancers, likely as a result of lineage-specific losses of enhancer activity. Finally, we show that some Ly49 genes can be cross-regulated by the enhancers of other Ly49 genes, suggesting that the Ly49 family have evolved a concerted regulatory mechanism. Collectively, we demonstrate the different modes of epigenetic evolution for a rapidly expanding gene family essential for host immunity, and provide a rich epigenetic dataset for NK cell research.
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Project description:Comparative genomics has revealed the rapid lineage-specific expansion of multiple gene families involved in immunity, presumably due to the complexity of ensuring pathogen defense while maintaining self-tolerance. Paralogs within these gene families often evolved distinct roles in immunity. However, less is known about how the epigenome and cis-regulation of these gene families evolved. Here we focus on the epigenetic evolution of the rapidly evolving murine Ly49 gene family. Ly49 genes mainly encode either inhibitory or activating surface receptors in natural killer (NK) cells. Together, they fine-tune NK cell activation. We systemically mapped Ly49 transcription initiation, chromatin accessibility, DNA methylation and 3D chromatin interactions. Our data revealed that each Ly49 gene forms a cis-regulatory unit consisted of one or more lowly accessible promoters and a proximal enhancer. Importantly, parallel to the functional divergence of the encoded proteins, inhibitory and activating Ly49 genes have evolved two separate sets of proximal enhancers, likely as a result of lineage-specific losses of enhancer activity. Finally, we show that some Ly49 genes can be cross-regulated by the enhancers of other Ly49 genes, suggesting that the Ly49 family have evolved a concerted regulatory mechanism. Collectively, we demonstrate the different modes of epigenetic evolution for a rapidly expanding gene family essential for host immunity, and provide a rich epigenetic dataset for NK cell research.
2024-04-20 | GSE226498 | GEO
Project description:Comparative genomics has revealed the rapid lineage-specific expansion of multiple gene families involved in immunity, presumably due to the complexity of ensuring pathogen defense while maintaining self-tolerance. Paralogs within these gene families often evolved distinct roles in immunity. However, less is known about how the epigenome and cis-regulation of these gene families evolved. Here we focus on the epigenetic evolution of the rapidly evolving murine Ly49 gene family. Ly49 genes mainly encode either inhibitory or activating surface receptors in natural killer (NK) cells. Together, they fine-tune NK cell activation. We systemically mapped Ly49 transcription initiation, chromatin accessibility, DNA methylation and 3D chromatin interactions. Our data revealed that each Ly49 gene forms a cis-regulatory unit consisted of one or more lowly accessible promoters and a proximal enhancer. Importantly, parallel to the functional divergence of the encoded proteins, inhibitory and activating Ly49 genes have evolved two separate sets of proximal enhancers, likely as a result of lineage-specific losses of enhancer activity. Finally, we show that some Ly49 genes can be cross-regulated by the enhancers of other Ly49 genes, suggesting that the Ly49 family have evolved a concerted regulatory mechanism. Collectively, we demonstrate the different modes of epigenetic evolution for a rapidly expanding gene family essential for host immunity, and provide a rich epigenetic dataset for NK cell research.
2024-04-20 | GSE226497 | GEO
Project description:Comparative genomics has revealed the rapid lineage-specific expansion of multiple gene families involved in immunity, presumably due to the complexity of ensuring pathogen defense while maintaining self-tolerance. Paralogs within these gene families often evolved distinct roles in immunity. However, less is known about how the epigenome and cis-regulation of these gene families evolved. Here we focus on the epigenetic evolution of the rapidly evolving murine Ly49 gene family. Ly49 genes mainly encode either inhibitory or activating surface receptors in natural killer (NK) cells. Together, they fine-tune NK cell activation. We systemically mapped Ly49 transcription initiation, chromatin accessibility, DNA methylation and 3D chromatin interactions. Our data revealed that each Ly49 gene forms a cis-regulatory unit consisted of one or more lowly accessible promoters and a proximal enhancer. Importantly, parallel to the functional divergence of the encoded proteins, inhibitory and activating Ly49 genes have evolved two separate sets of proximal enhancers, likely as a result of lineage-specific losses of enhancer activity. Finally, we show that some Ly49 genes can be cross-regulated by the enhancers of other Ly49 genes, suggesting that the Ly49 family have evolved a concerted regulatory mechanism. Collectively, we demonstrate the different modes of epigenetic evolution for a rapidly expanding gene family essential for host immunity, and provide a rich epigenetic dataset for NK cell research.
2024-04-20 | GSE226500 | GEO
Project description:Comparative genomics has revealed the rapid lineage-specific expansion of multiple gene families involved in immunity, presumably due to the complexity of ensuring pathogen defense while maintaining self-tolerance. Paralogs within these gene families often evolved distinct roles in immunity. However, less is known about how the epigenome and cis-regulation of these gene families evolved. Here we focus on the epigenetic evolution of the rapidly evolving murine Ly49 gene family. Ly49 genes mainly encode either inhibitory or activating surface receptors in natural killer (NK) cells. Together, they fine-tune NK cell activation. We systemically mapped Ly49 transcription initiation, chromatin accessibility, DNA methylation and 3D chromatin interactions. Our data revealed that each Ly49 gene forms a cis-regulatory unit consisted of one or more lowly accessible promoters and a proximal enhancer. Importantly, parallel to the functional divergence of the encoded proteins, inhibitory and activating Ly49 genes have evolved two separate sets of proximal enhancers, likely as a result of lineage-specific losses of enhancer activity. Finally, we show that some Ly49 genes can be cross-regulated by the enhancers of other Ly49 genes, suggesting that the Ly49 family have evolved a concerted regulatory mechanism. Collectively, we demonstrate the different modes of epigenetic evolution for a rapidly expanding gene family essential for host immunity, and provide a rich epigenetic dataset for NK cell research.
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