CRNKL1 Is a Highly Selective Regulator of Intron-Retaining HIV-1 and Cellular mRNAs
Han Xiao, Emanuel Wyler, Miha Milek, Bastian Grewe, Philipp Kirchner, Arif B. Ekici, Ana Beatriz Oliveira Villela Silva, Doris Jungnickl, Florian Full, Marco Thomas, Markus Landthaler, Armin Ensser, Klaus Überla
Abstract
To regulate its complex splicing pattern, HIV-1 uses the adaptor protein Rev to shuttle unspliced or partially spliced mRNA from the nucleus to the cytoplasm. In the absence of Rev, these RNAs are retained in the nucleus, but it is unclear why. Here we identify cellular proteins whose depletion enhances cytoplasmic levels of the HIV-1 unspliced RNA. Depletion of one of them, CRNKL1, also increases cytoplasmic levels of a subset of intron-retaining cellular mRNA, suggesting that CRNKL1-dependent nuclear retention may be a basic cellular mechanism exploited by HIV-1.