Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ATAC-Seq)

Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during drug resistance, but the underlying mechanisms are not fully understood. Here we demonstrate that HP1g coordinates histone H3 lysine 9 trimethylation (H3K9me3) to regulate chromatin dynamic and gene transcription during bortezomib resistance.Mechanistically, HP1g can interact with H3K9me3, its CD domain is responsible to read H3K9me3 to serve its function. Overall design: ATAC-seq analysis from WT or BR LP-1 cells and cells infected with overexpression HP1g plasmid or vector. Cells were harvested for chromatin accessibility profiling. Two replicates were performed per sample.