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Molecular and Cellular Biology, January 2007, p. 699-708, Vol. 27, No. 2
0270-7306/07/$08.00+0     doi:10.1128/MCB.01572-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The doublesex Splicing Enhancer Components Tra2 and Rbp1 Also Repress Splicing through an Intronic Silencer{triangledown}

Junlin Qi, Shihuang Su, and William Mattox*

Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, and Genes and Development Graduate Program, The University of Texas Graduate School of Biomedical Sciences, 1515 Holcombe Blvd., Houston, Texas 77030-4009

Received 22 August 2006/ Returned for modification 3 October 2006/ Accepted 27 October 2006

The activation of sex-specific alternative splice sites in the Drosophila melanogaster doublesex and fruitless pre-mRNAs has been well studied and depends on the serine-arginine-rich (SR) splicing factors Tra, Tra2, and Rbp1. Little is known, however, about how SR factors negatively regulate splice sites in other RNAs. Here we examine how Tra2 blocks splicing of the M1 intron from its own transcript. We identify an intronic splicing silencer (ISS) adjacent to the M1 branch point that is sufficient to confer Tra2-dependent repression on another RNA. The ISS was found to function independently of its position within the intron, arguing against the idea that bound repressors function by simply interfering with branch point accessibility to general splicing factors. Conserved subelements of the silencer include five short repeated sequences that are required for Tra2 binding but differ from repeated binding sites found in Tra2-dependent splicing enhancers. The ISS also contains a consensus binding site for Rbp1, and this protein was found to facilitate repression of M1 splicing both in vitro and in Drosophila larvae. In contrast to the cooperative binding of SR proteins observed on the doublesex splicing enhancer, we found that Rbp1 and Tra2 bind to the ISS independently through distinct sequences. Our results suggest that functionally synergistic interactions of these SR factors can cause either splicing activation or repression.

* Corresponding author. Mailing address: Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030-4009. Phone: (713) 834-6329. Fax: (713) 834-6339. E-mail: wmattox{at}mdanderson.org.

{triangledown} Published ahead of print on 13 November 2006.

Molecular and Cellular Biology, January 2007, p. 699-708, Vol. 27, No. 2
0270-7306/07/$08.00+0     doi:10.1128/MCB.01572-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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