Hepatocyte nuclear factor-1β recruits the nucleosome remodeling and deacetylase complex to activate gene transcription

Endogenous HNF-1β recruits NuRD in wild-type renal epithelial cells, colocalizing at 2,776 intergenic/intronic sites and enabling NuRD-dependent chromatin opening at 113 sites.

• Why it matters: The mechanism by which HNF-1β regulates gene transcription in renal epithelial cells is unclear, despite its mutations being the most common monogenic cause of congenital anomalies of the kidney and urinary tract.
• What they did: An unbiased proteomic screen identified endogenous HNF-1β interactions with NuRD core subunits, and genome-wide ChIP-seq showed colocalization with GATAD2A, CHD4, and MBD3 at 2,776 sites.
• The result: NuRD co-occupancy at 628 sites (22.6%) was reduced without HNF-1β, and 113 sites (18.2%) showed higher ATAC-seq peaks and increased H3K27 acetylation, with CHD4 knockdown reducing 67 HNF-1β-regulated genes.