Long noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. This study shows that the lincRNA HOTAIR serves as a scaffold for two distinct histone modification complexes: Polycomb Repressive Complex 2 (PRC2) and the LSD1/CoREST/REST complex. The 5' domain of HOTAIR binds PRC2, while the 3' domain binds the LSD1 complex. This allows RNA-mediated assembly of PRC2 and LSD1, coordinating their targeting to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. The results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes. HOTAIR is transcribed from the HOXC locus and targets PRC2 to silence HOXD and other genes. It also binds to CoREST/REST repressor complexes, which contain LSD1, a demethylase that mediates enzymatic demethylation of H3K4me2. The study hypothesizes that HOTAIR may coordinately interact with both PRC2 and LSD1. Immunoprecipitation experiments show that HOTAIR specifically binds to both complexes. Further, biotinylated HOTAIR binds to purified PRC2 and LSD1 complexes in vitro. These results suggest that HOTAIR directly interacts with PRC2 and LSD1 complexes. Using deletion mutants, the PRC2 binding activity of HOTAIR maps to nucleotides 1 to 300, while the LSD1 complex binding activity maps to nucleotides 1500 to 2146. Deletion mutants that retain these regions bind to PRC2 or LSD1 complexes with equal efficiency as full-length HOTAIR. These findings indicate that HOTAIR is a modular bifunctional RNA with distinct binding domains for PRC2 and LSD1 complexes. HOTAIR-mediated bridging of PRC2 and LSD1 complexes enables their coordinate binding to target genes on chromatin. HOTAIR is required for H3K27 methylation and transcriptional silencing across the HOXD locus. ChIP-chip analysis shows that PRC2 and LSD1 occupy 4740 and 2116 gene promoters, respectively. Nearly one third of LSD1 occupied promoters are also occupied by SUZ12, revealing a significant overlap. HOTAIR knockdown leads to concordant loss of SUZ12 and LSD1 occupancy in 289 of the 721 genes normally co-occupied by SUZ12 and LSD1. These results suggest that HOTAIR is required to target both PRC2 and LSD1 to hundreds of genes across the genome to coordinate histone modifications for gene silencingLong noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. This study shows that the lincRNA HOTAIR serves as a scaffold for two distinct histone modification complexes: Polycomb Repressive Complex 2 (PRC2) and the LSD1/CoREST/REST complex. The 5' domain of HOTAIR binds PRC2, while the 3' domain binds the LSD1 complex. This allows RNA-mediated assembly of PRC2 and LSD1, coordinating their targeting to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. The results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes. HOTAIR is transcribed from the HOXC locus and targets PRC2 to silence HOXD and other genes. It also binds to CoREST/REST repressor complexes, which contain LSD1, a demethylase that mediates enzymatic demethylation of H3K4me2. The study hypothesizes that HOTAIR may coordinately interact with both PRC2 and LSD1. Immunoprecipitation experiments show that HOTAIR specifically binds to both complexes. Further, biotinylated HOTAIR binds to purified PRC2 and LSD1 complexes in vitro. These results suggest that HOTAIR directly interacts with PRC2 and LSD1 complexes. Using deletion mutants, the PRC2 binding activity of HOTAIR maps to nucleotides 1 to 300, while the LSD1 complex binding activity maps to nucleotides 1500 to 2146. Deletion mutants that retain these regions bind to PRC2 or LSD1 complexes with equal efficiency as full-length HOTAIR. These findings indicate that HOTAIR is a modular bifunctional RNA with distinct binding domains for PRC2 and LSD1 complexes. HOTAIR-mediated bridging of PRC2 and LSD1 complexes enables their coordinate binding to target genes on chromatin. HOTAIR is required for H3K27 methylation and transcriptional silencing across the HOXD locus. ChIP-chip analysis shows that PRC2 and LSD1 occupy 4740 and 2116 gene promoters, respectively. Nearly one third of LSD1 occupied promoters are also occupied by SUZ12, revealing a significant overlap. HOTAIR knockdown leads to concordant loss of SUZ12 and LSD1 occupancy in 289 of the 721 genes normally co-occupied by SUZ12 and LSD1. These results suggest that HOTAIR is required to target both PRC2 and LSD1 to hundreds of genes across the genome to coordinate histone modifications for gene silencing