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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Spatial interplay between Polycomb and Trithorax complexes controls transcriptional activity in T lymphocytes

ABSTRACT: Trithorax group (TrxG) and Polycomb group (PcG) proteins are two mutually antagonistic chromatin modifying complexes, however, how they together mediate transcriptional counterregulation remains unknown. Genome-wide analysis revealed that binding of Ezh2 and Menin, central members of the PcG and TrxG complexes, respectively, were reciprocally correlated. Moreover, we identified a developmental change in the positioning of Ezh2 and Menin in differentiated T lymphocytes compared to embryonic stem cells. Ezh2-binding upstream and Menin-binding downstream of the transcription start site (TSS) was frequently found at genes with higher transcriptional levels, and Ezh2-binding downstream and Menin-binding upstream was found at genes with lower expression in T lymphocytes. Interestingly, of the Ezh2 and Menin co-occupied genes, those exhibiting occupancy at the same position displayed greatly enhanced sensitivity to loss of Ezh2. Finally, we also found that different combinations of Ezh2 and Menin occupancy were associated with expression of specific functional gene groups important for T cell development. Therefore, spatial cooperative gene regulation by the PcG and TrxG complexes may represent a novel mechanism regulating the transcriptional identity of differentiated cells. ES cells, B cells and T cells are profiled for mRNA expression

ORGANISM(S): Mus musculus

SUBMITTER: Atsushi Onodera

PROVIDER: E-GEOD-72757 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Spatial interplay between Polycomb and Trithorax complexes controls transcriptional activity in T lymphocytes [ChIP-Seq]

Project description:Trithorax group (TrxG) and Polycomb group (PcG) proteins are two mutually antagonistic chromatin modifying complexes, however, how they together mediate transcriptional counterregulation remains unknown. Genome-wide analysis revealed that binding of Ezh2 and Menin, central members of the PcG and TrxG complexes, respectively, were reciprocally correlated. Moreover, we identified a developmental change in the positioning of Ezh2 and Menin in differentiated T lymphocytes compared to embryonic stem cells. Ezh2-binding upstream and Menin-binding downstream of the transcription start site (TSS) was frequently found at genes with higher transcriptional levels, and Ezh2-binding downstream and Menin-binding upstream was found at genes with lower expression in T lymphocytes. Interestingly, of the Ezh2 and Menin co-occupied genes, those exhibiting occupancy at the same position displayed greatly enhanced sensitivity to loss of Ezh2. Finally, we also found that different combinations of Ezh2 and Menin occupancy were associated with expression of specific functional gene groups important for T cell development. Therefore, spatial cooperative gene regulation by the PcG and TrxG complexes may represent a novel mechanism regulating the transcriptional identity of differentiated cells.

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An essential role for PTIP in mediating Hox gene regulation along PcG and trxG pathways

Project description:During Drosophila development, Polycomb-group and Trithorax-group proteins function to ensure correct maintenance of transcription patterns by epigenetically repressing or activating target gene expression. To get a deep insight into the PcG and trxG pathways, we investigated a BRCT domain-containing protein called PTIP, which was generally identified as a transcriptional coactivator and belongs to the TRR complex. At the genome scale, we sorted given PTIP binding peaks into two groups: PTIP/TRR-cobound and PTIP/PC-cobound peaks. In particular, we found that PTIP mediates the molecular switch between H3K4me3/H3K27ac and H3K27me3 histone modifications at TRR or PC occupied regions. Thus, we suggest that PTIP is a mediator rather than a dedicated co-activator along PcG and trxG pathways. Our hypothesis is further supported by the genetic assay: PTIP interacts genetically with either PcG or TrxG in a dosage-dependent manner, suggesting that PTIP functions as a co-factor of PcG/TrxG proteins. In addition, in accordance with the analysis of ChIP-seq, these genetic interactions correlate with modified ectopic HOX protein levels in imaginal discs, which reveals an essential role for PTIP in PcG-mediated Hox gene repression. Hence, we reveal a novel role for PTIP in the epigenetic regulation of gene expression along PcG and trxG pathways.

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