Ddx10 functions as a positive regulator of somatic cell reprogramming

RNA-binding proteins (RBPs) function in all steps of cellular RNA metabolism. Here, we find that Ddx10 gain-of-function promotes but loss-of-function impedes somatic cell reprogramming. Ddx10 loss-of-function results in significantly abnormal expression of innate immune response genes at the late stage of reprogramming. Knockdown of interferon transcription factor Irf1 or its downstream targets, Igtp and Tgtp2, respectively, obviously inhibited reprogramming. This study revealed that Ddx10 regulated reprogramming through modulating innate immune network. Overall design: Gene expression profiling of reprogrammed cells with OSKM plus control shRNA or Ddx10 shRNAs at different time points. Each experiment was done in biological replicates.