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J. Biol. Chem., Vol. 277, Issue 47, 45172-45180, November 22, 2002

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Differential Splicing Generates Tvl-1/RFXANK Isoforms with Different Functions^*

Santasabuj Das^§, Jun-Hsiang Lin^¶, Joseph Papamatheakis, Yuri Sykulev, and Philip N. Tsichlis^**

From the  Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 and the  Foundation for Research and Technology, Institute of Molecular Biology and Biotechnology, Heraklion, 711 10 Crete, Greece

Earlier studies have shown that Tvl-1 gives rise to at least two differentially spliced mRNAs, one of which (Tvl-S) encodes a protein that lacks amino acids 91-112. DNA binding of RFX complexes assembled in the presence of Tvl-S is impaired. As a result, Tvl-S does not support the expression of Class II major histocompatibility complex (MHC) genes. Here, we show that the reason Tvl-S is inactive as a transcriptional regulator of Class II MHC genes is that the RFX complexes assembled in the presence of Tvl-S are unstable. Additionally, we show that interferon-, which induces Class II MHC gene expression in 293 cells, promotes a shift in the splicing pattern of RFXANK/Tvl-1 toward the transcriptionally active Tvl-L isoform, suggesting that differential splicing of Tvl-1 is a signal-regulated process. Finally, we show that Tvl-1 regulates the expression of non-MHC genes. One such gene encodes the ephrin receptor EphA3. Since both Tvl-L and Tvl-S are identical in their ability to induce the expression of EphA3, we conclude that Tvl-1 regulates the expression of non-MHC genes by RFX-independent mechanisms.

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