U2AF1 mutation causes an oxidative stress and DNA repair defect in hematopoietic and leukemic cells
U2AF1 is a core component of spliceosome and controls cell-fate specific alternative splicing. U2AF1 mutations have been frequently identified in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients, and mutations in U2AF1 are associated with poor prognosis in hematopoietic malignant diseases. To investigate the effects of U2af1 S34F in hematopoietic cells, we performed global gene expression profiling by RNA sequencing on U2af1-WT and U2af1 S34F 32D cells. We find that U2AF1 S34F causes increased reactive oxygen species (ROS) production. In hematopoietic cell line, a defect in mitochondrial function and DNA damage response deficiency are found in U2AF1 S34F expressing 32D cells. Overall design: Transcriptome sequencing of U2af1-WT and U2af1 S34F 32D cells.