Genomic binding of NF-Y in mouse and human cells

Area of Science:

• Molecular Biology
• Genomics
• Epigenetics

Background:

• NF-Y is a crucial transcription factor that binds to the CCAAT-box motif.
• Understanding NF-Y's regulatory mechanisms is vital for comprehending gene expression control.

Purpose of the Study:

• To elucidate the genome-wide binding strategy of NF-Y across different mammalian cell types.
• To investigate the functional relationship between NF-Y and its co-factor USF1 at target loci.

Main Methods:

• Analysis of 16 ChIP-seq datasets from human and mouse cells.
• Identification of shared and cell-type-specific NF-Y binding sites.
• Assessment of histone modifications and co-factor binding at NF-Y loci.
• Evaluation of USF1 binding upon NF-YB inactivation.

Main Results:

• NF-Y commonly binds to promoters of actively transcribed genes involved in cell cycle, metabolism, and gene expression.
• NF-Y also binds to enhancers and specific retroviral-like Transposable Elements (TEs).
• USF1 binding is significantly reduced at promoters but only modestly affected at MLT1 TEs after NF-YB inactivation.

Conclusions:

• NF-Y targets a conserved set of functional loci across mammalian cells.
• NF-Y exhibits a pioneering role at gene promoters, facilitating chromatin accessibility.
• NF-Y's role at Transposable Elements differs from its role at promoters, suggesting distinct regulatory mechanisms.