Loss of ADAR1 in human iPS cells promotes caspase3-mediated apoptotic cell death.

Abstract

Adenosine deaminases acting on RNA (ADARs) convert adenosine residues to inosine specifically in double-stranded RNAs. In this study, we investigated the function of primary RNA editing enzyme ADAR1 in pluripotent stem cells and found that loss of ADAR1 in human iPS cells promotes caspase3-mediated cell death. However, ADAR1 knockdown (KD) did not alter cell morphology, alkaline phosphatase (AP) staining activities and the expression levels of pluripotent marker genes, indicating that ADAR1 is dispensable for maintenance of pluripotency. Furthermore, ADAR1-KD iPS cells did not change proliferation rate. These findings extended the role of ADAR1 and might open the road for understanding pluripotent state more deeply.