Abstract The NF-Y (HAP2/3/5 or CCAAT-binding factor) complex is an evolutionarily conserved heterotrimeric transcription factor (TF) that binds the CCAAT box in ∼30% of eukaryotic promoters. While NF-Y alters chromatin structure, its mechanisms remain enigmatic. In Penicillium oxalicum and Trichoderma reesei, near-complete chromatin remodeling complexes (CRCs) SWI/SNF and RSC were captured using NF-Y subunits as bait. Resolution of the structural compositions of SWI/SNF and RSC in both fungi revealed four novel filamentous-fungi-specific subunits: SWI/SNF-specific Fif1/Fif2 and RSC-specific Fif3/Fif4. These subunits distinguish filamentous fungal SWI/SNF and RSC from their counterparts in unicellular yeast and multicellular metazoans. SWI/SNF subunits (Snf19/Sol1/Fif1) and RSC subunits (Rsc7/Fif3) serve as direct targets for NF-Y-CRC interaction. Functional studies of the P. oxalicum NF-Y subunits PoNF–YB and PoNF–YC, along with the SWI/SNF–specific PoFif1 and the RSC–specific PoFif3, revealed their overlapping yet distinct roles in fungal growth, development, and cell wall-degrading enzyme production. The chromatin occupancy of PoFif1 and PoFif3 at certain target promoters is PoNF–Y-dependent. These findings suggest a model in which NF-Y interacts with the CRCs to coordinately regulate these growth, developmental, and metabolic processes. This model may explain how a canonical TF exhibits “pseudo-chromatin remodeler” activity: through its engagement with authentic CRCs, namely, SWI/SNF and RSC.
Ma et al. (Wed,) studied this question.