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Papers In Press, published online ahead of print October 22, 2001
J. Biol. Chem, 10.1074/jbc.M109018200
Submitted on September 18, 2001
Revised on October 12, 2001
Accepted on October 22, 2001

The EWS/NOR1 fusion gene product gains a novel activity affecting pre-mRNA splicing

Naganari Ohkura, Hiroko Yaguchi, Toshihiko Tsukada, and Ken Yamaguchi

Growth Factor Division, National Cancer Center Research Institute, Tokyo 104-0045

Corresponding Author: nohkura{at}gan2.ncc.go.jp

In extraskeletal myxoid chondrosarcoma, the chromosomal translocation creates a gene fusion between EWS and an orphan nuclear receptor NOR1. The resulting fusion gene product, EWS/NOR1, has been believed to lead to malignant transformation by functioning as a transcriptional activator, but an alternative mechanism may also be involved. Here, using a newly developed functional complementation screening in yeast, we found that EWS/NOR1, but not EWS or NOR1, complemented the loss of function of the small nuclear ribonucleoprotein Snu23, an essential factor for pre-mRNA splicing in yeast. To verify the potential function of EWS/NOR1 in mammalian cells, we next showed that overexpression of EWS/NOR1 caused increased usage of the distal 5’ splice site of the pre-mRNA splicing, and that EWS/NOR1 interacted with a human splicing protein U1C; neither EWS nor NOR1 had the same activity or interaction as EWS/NOR1. Altogether, our findings reveal that EWS/NOR1 gains a novel activity affecting the pre-mRNA splicing.


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