Abstract
THE adenovirus L1 unit1 represents an example of an alternatively spliced precursor messenger (pre-mRNA) where one 5' splice can be joined to one of two alternative 3' splice sites, producing the 52,55K or the IIIa mRNAs (Fig. 1a). Efficient usage of the distal IIIa 3' splice site requires late viral protein synthesis and is therefore confined to the late phase of virus infection2–4. Here we show that, in extracts from uninfected cells, the classical SR proteins5, which are essential splicing factors5–7, inhibit IIIa pre-mRNA splicing by binding to an intronic repressor element and preventing recruitment of the U2 small nuclear ribonucleoprotein particle to the spliceosome. We further show that the viral repressor element has splicing-enhancer activity when appropriately placed in the pre-mRNA. Together, our results demonstrate that SR proteins function as activators or repressors of splicing depending on where on the pre-mRNA they bind.
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Kanopka, A., Mühlemann, O. & Akusjärvi, G. Inhibition by SR proteins of splicing of a regulated adenovirus pre-mRNA. Nature 381, 535–538 (1996). https://doi.org/10.1038/381535a0
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DOI: https://doi.org/10.1038/381535a0
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