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Tnpo3 controls splicing of the pre-mRNA encoding the canonical TCR α chain of iNKT cells

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Iwanami,  Norimasa
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Richter,  Andreas S
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Sikora,  Katarzyna
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons190993

Boehm,  Thomas
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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10.1038_s41467-023-39422-4.pdf
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Citation

Iwanami, N., Richter, A. S., Sikora, K., & Boehm, T. (2023). Tnpo3 controls splicing of the pre-mRNA encoding the canonical TCR α chain of iNKT cells. Nature Communications, 14: 3645. doi:10.1038/s41467-023-39422-4.


Cite as: https://hdl.handle.net/21.11116/0000-000D-4F8C-E
Abstract
Unconventional T cells, such as innate natural killer T cells (iNKT) cells, are an important part of vertebrate immune defences. iNKT recognise glycolipids through a T cell receptor (TCR) that is composed of a semi-invariant TCR α chain, paired with a restricted set of TCR β chains. Here, we show that splicing of the cognate Trav11-Traj18-Trac pre-mRNA encoding the characteristic Vα14Jα18 variable region of this semi-invariant TCR depends on the presence of Tnpo3. The Tnpo3 gene encodes a nuclear transporter of the β-karyopherin family whose cargo includes various splice regulators. The block of iNKT cell development in the absence of Tnpo3 can be overcome by transgenic provision of a rearranged Trav11-Traj18-Trac cDNA, indicating that Tnpo3 deficiency does not interfere with the development of iNKT cells per se. Our study thus identifies a role for Tnpo3 in regulating the splicing of the pre-mRNA encoding the cognate TCRα chain of iNKT cells.