Nucleic Acids Research Advance Access originally published online on February 3, 2009
Nucleic Acids Research 2009 37(6):1907-1914; doi:10.1093/nar/gkp050
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Nucleic Acids Research, 2009, Vol. 37, No. 6 1907-1914
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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U1-independent pre-mRNA splicing contributes to the regulation of alternative splicing
1Department of Biology, Graduate School of Science, Kobe University, 1-1 Rokkodaicho, Nadaku, Kobe 657-8501, 2Institute for Virus Research, Kyoto University, Kyoto 606-8507 and 3Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan
*To whom correspondence should be addressed. Tel: +81 78 803 5725; Fax: +81 78 803 5725; Email: kunio{at}kobe-u.ac.jp
Received September 26, 2008. Revised January 13, 2009. Accepted January 16, 2009.
U1 snRNP plays a crucial role in the 5' splice site recognition during splicing. Here we report the first example of naturally occurring U1-independent U2-type splicing in humans. The U1 components were not included in the pre-spliceosomal E complex formed on the human F1
(hF1
) intron 9 in vitro. Moreover, hF1
intron 9 was efficiently spliced even in U1-disrupted Xenopus oocytes as well as in U1-inactivated HeLa nuclear extracts. Finally, hF1
exon 9 skipping induced by an alternative splicing regulator Fox-1 was impaired when intron 9 was changed to the U1-dependent one. Our results suggest that U1-independent splicing contributes to the regulation of alternative splicing of a class of pre-mRNAs.