GSE138093
Different response to oxidative damage of iPS cells and the progenitor fibroblast cells through the lens of the DNA repair system
In response to DNA damage, cells arrest the cell cycle to repair damage, induce apoptosis when unrepaired, and avoid the accumulation of mutations. Our present analysis showed that oxidative stress causing DNA damage in the same condition resulted in apoptosis in induced pluripotent stem cells (iPSCs), but background levels of apoptosis in progenitor fibroblasts that just suffered cell-cycle arrest. PCA analysis of RNA-seq data and annexin V staining revealed apoptosis in iPSCs recovered within 24 hours. Characteristics as a stem cell obtained by reprogramming have shown that systems have been established that do not leave mutations in daughter cells by quickly induced apoptosis when accurate DNA repair was impossible. The surviving cells' gene expression reverts to approximately the same as that before oxidative damage in 24 hours, although the expression of error-free DNA repair-related genes has not reverted. On the other hand, the expression of error-prone polymerase POLH and REV3 revealed up-regulation. This pattern might cause the possibility of mutation in the genome after oxidative stress. Overall design: RNA-sequencing analyses were performed in three fibroblast cells and one its-derived induced pluripotent stem cells.