Project description:We report the application of ChIP-Seq technology for analyzing the DNA binding sites of SOD1 in the nucleus of HeLa cells. By obtaining a plenty of sequence from chromatin immunoprecipitated DNA, we generated genome-wide DNA binding sites of SOD1. After sequencing of ChIP samples, 42,737,195, 49,950,032, and 38,825,768 clean reads for control group, H2O2 treated group and LD100 (a specific inhibitor of SOD1) treated group were obtained through trimming the raw reads. We find that SOD1 occupies DNA sites with distinct sequence preference in the nucleus. The treatment with either H2O2 or LD100 was found to decrease the strength of SOD1 binding to DNA, indicating that the H2O2 exposure- or SOD1 inhibition-mediated redox dyshomeostasis may result in decreased genes that are reasonably regulated through alteration of SOD1 structures compared to control.
Project description:We report the application of ATACseq to differentiating ATDC5 cells with the aim of identifying how chromatin architecture is changing as these cells move from pre-chondrocytes to differentiated chondrocytes. Raw data was generated by sequencing using the Novaseq6000 with 50bp single end reads. Trimming to remove adapters or poor-quality reads was performed with no sequence below 30 nucleotides in length used in the analysis. We found that there were significant changes in chromatin accessibility at both days 3 and 10 of differentiation. Using diffBind, differential peaks were identified at day 3 and 10. These peaks were further analyzed for enriched transcription factor binding sites and identified motifs for the RUNX family transcription factors as well as SOX9.
