Project description:This SuperSeries is composed of the following subset Series: GSE22343: ChIP-chip of siGFP- or siHOTAIR-treated foreskin fibroblasts with anti-H3K4me2, anti-LSD1 or anti-SUZ12 antibodies on HOX tiling array GSE22344: ChIP-chip of siGFP- or siHOTAIR-treated foreskin fibroblasts with anti-LSD1 or anti-SUZ12 antibodies on human HG18 Nimblegen promoter arrays Refer to individual Series
Project description:Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5’ domain of HOTAIR binds Polycomb Repressive Complex 2 (PRC2) while a 3’ domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1, and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, and thereby specify the pattern of histone modifications on target genes. LSD1 and SUZ12 co-occupied on 721 genes in human foreskin fibroblasts. Coordinate loss of SUZ12 and LSD1 occupancy was caused by HOTAIR knockdown. Comparison occupancy of LSD1 and SUZ12 of siGFP and siHOTAIR foreskin fibroblasts on human HG18 promoter arrays. Human foreskin fibroblasts were transfected with siGFP or siHOTAIR. The cells were harvested and ChIP analysis with anti-LSD1 and anti-SUZ12 antibodies was performed.
Project description:Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5’ domain of HOTAIR binds Polycomb Repressive Complex 2 (PRC2) while a 3’ domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1, and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, and thereby specify the pattern of histone modifications on target genes. Coordinate loss of SUZ12 and LSD1 occupancy caused by HOTAIR knockdown were concentrated in proximal promoters of HOXD genes. These regions correspondingly lost H3K27me3 and gained H3K4me2, the respective histone methylation products of PRC2 and LSD1 complexes. Comparison occupancy of LSD1 and SUZ12 of siGFP and siHOTAIR foreskin fibroblasts on HOX tiling array. Human foreskin fibroblasts were transfected with siGFP or siHOTAIR. The cells were harvested and ChIP analysis with anti-H3K4me2, anti-LSD1 and anti-SUZ12 antibodies was performed.
Project description:ChIP-chip of siGFP- or siHOTAIR-treated foreskin fibroblasts with anti-H3K4me2, anti-LSD1 or anti-SUZ12 antibodies on HOX tiling array
Project description:Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5’ domain of HOTAIR binds Polycomb Repressive Complex 2 (PRC2) while a 3’ domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1, and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, and thereby specify the pattern of histone modifications on target genes. LSD1 and SUZ12 co-occupied on 721 genes in human foreskin fibroblasts. Coordinate loss of SUZ12 and LSD1 occupancy was caused by HOTAIR knockdown.
Project description:To identify genomic binding regions, THP1 AML cells were subjected to ChIP sequencing (ChIPseq) using anti-LSD1, MYB or GFI1 antibodies.
