Genome wide analsis of the chromatin accessibility and gene expression in control and NUDT5 depleted U2OS cells [ATAC-seq]

NUDT5 was reported to generate ATP to support local chromatin remodeling and transcription of hormone-responsive genes. Our research has found that NUDT5 is also required for DNA damage repair by homologous recombination. To investigate how NUDT5 regulates HR, we depleted NUDT5 in U2OS cells by siRNA and compared the transcriptome profiling (RNA-seq) of NUDT5 depleted cells with control cells to investigate whether NUDT5 regulate HR by altering the expression of essential components of the HR machinery. The results suggest that NUDT5 does not regulate HR by altering the expression of essential components of the HR machinery. To investigate whether NUDT5 contributes to chromatin remodeling after DNA damage, we compared the chromatin accessibility profiling (ATAC-seq) in NUDT5 depleted U2OS cells and control cells, either before or after ionizing radiation. The results suggest that NUDT5 silencing blocked most DNA damage-induced changes in chromatin accessibility following radiation exposure and implies that NUDT5 may support the activity of remodeling ATPases during damage repair. Overall design: RNA-seq analysis of U2OS cells transfected with siCtrl or siNUDT5 (samples in triplicate). ATAC-seq analysis of U2OS cells transfected with siCtrl or siNUDT5, treated with or without ionizing radiation at 5Gy (samples in duplicate).