Author: ["K. Nicole Clouse","Ming-juan Luo","Zhaolan Zhou","Robin Reed"]
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Abstract
All major nuclear export pathways so far examined follow a general paradigm1,2,3. Specifically, a complex is formed in the nucleus, containing the export cargo, a member of the importin-β family of transporters and RanGTP. This complex is translocated across the nuclear pore to the cytoplasm, where hydrolysis of the GTP on Ran is stimulated by the GTPase-activating protein RanGAP4,5. The activity of RanGAP is increased by RanBP1, which also promotes disassembly of RanGTP–cargo–transporter complexes6,7. Here we investigate the role of RanGTP in the export of mRNAs generated by splicing. We show that nuclear injection of a Ran mutant (RanT24N)8 or the normally cytoplasmic RanGAP potently inhibits the export of both tRNA and U1 snRNA9, but not of spliced mRNAs. Moreover, nuclear injection of RanGAP together with RanBP1 blocks tRNA export but does not affect mRNA export. These and other data indicate that export of spliced mRNA is the first major cellular transport pathway that is independent of the export co-factor Ran.
Cite this article
Clouse, K., Luo, Mj., Zhou, Z. et al. A Ran-independent pathway for export of spliced mRNA. Nat Cell Biol 3, 97–99 (2001). https://doi.org/10.1038/35050625