MRT, Functioning with NURF Complex, Regulates Lipid Droplet Size

Summary Lipid droplets (LDs) are highly dynamic organelles that store neutral lipids. Through a gene overexpression screen in the Drosophila larval fat body, we have identified that MRT, an Myb/switching-defective protein 3 (Swi3), Adaptor 2 (Ada2), Nuclear receptor co-repressor (N-CoR), Transcription factor (TF)IIIB (SANT)-like DNA-binding domain-containing protein, regulates LD size and lipid storage. MRT directly interacts with, and is functionally dependent on, the PZG and NURF chromatin-remodeling complex components. MRT binds to the promoter of plin1 , the gene encoding the LD-resident protein perilipin, and inhibits the transcription of plin1 . In vitro LD coalescence assays suggest that mrt overexpression or loss of plin1 function facilitates LD coalescence. Our findings suggest that MRT functions together with chromatin-remodeling factors to regulate LD size, likely through the transcriptional repression of plin1 .