Genomic binding of NF-Y in mouse and human cells

Le résumé fourni par la source

NF-Y is a Transcription Factor that regulates transcription through binding to the CCAAT-box. To understand its strategy, we analyzed 16 ChIP-seq datasets from human and mouse cells. Shared loci, mostly located in promoters of expressed genes of cell cycle , metabolism and gene expression pathways, are associated with histone marks of active chromatin and specific modules of TFs. Other peaks are in enhancers and Transposable Elements -TE- of retroviral origin in human and mouse. We evaluated the relationship with USF1, a common synergistic partner in promoters and MLT1 TEs, upon NF-YB inactivation: USF1 binding decreases in promoters, modestly in MLT1, suggesting a pioneering role of NF-Y in formers, not in the latters. These data define a common set of NF-Y functional targets across different mammalian cell types, suggesting a pioneering role in promoters with respect to TEs. • NF-Y has a general preference for promoters, in mouse and human cell lines. • NF-Y target genes are of cell cycle, gene expression and metabolism pathways. • NF-Y removal entails a decrease of USF1 binding in promoters, less in repeats. • NF-YB inactivation leads to a drop in expression of USF1 + /NF-Y + targeted genes.

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