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. 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.