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Titolo:
U1 small nuclear ribonucleoprotein and splicing inhibition by the Rous sarcoma virus negative regulator of splicing element
Autore:
McNally, LM; McNally, MT;
Indirizzi:
Med Coll Wisconsin, Dept Microbiol & Mol Genet, Milwaukee, WI 53226 USA Med Coll Wisconsin Milwaukee WI USA 53226 Genet, Milwaukee, WI 53226 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 3, volume: 73, anno: 1999,
pagine: 2385 - 2393
SICI:
0022-538X(199903)73:3<2385:USNRAS>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA INTRONS; AT-AC INTRONS; UNSPLICED RNA; SR PROTEINS; MINOR CLASS; IN-VIVO; TYPE-1; REPLICATION; CIS; SITES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: McNally, MT Medlwaukee,sconsin, Dept Microbiol & Mol Genet, 8701 WatertownPlank Rd, Mi Med Coll Wisconsin 8701 Watertown Plank Rd Milwaukee WI USA 53226
Citazione:
L.M. McNally e M.T. McNally, "U1 small nuclear ribonucleoprotein and splicing inhibition by the Rous sarcoma virus negative regulator of splicing element", J VIROLOGY, 73(3), 1999, pp. 2385-2393

Abstract

Retroviruses require both spliced and unspliced RNA for replication, Accumulation of unspliced Rous sarcoma virus RNA is facilitated in part by a negative cis element in the gag region, termed the negative regulator of splicing (NRS), which serves to repress splicing of viral RNA but can also blocksplicing of heterologous introns, The NRS binds components of the splicingmachinery including SR proteins, U1 and U2, small nuclear ribonucleoproteins (snRNPs) of the major splicing pathway, and U11 snRNP of the minor pathway, yet splicing does not normally occur from the NRS. A mutation that abolishes U11 binding (RG11) also abrogates NRS splicing inhibition, indicatingthat U11 is functionally important for NRS activity and suggesting that the NRS is recognized as a minor-class 5' splice site (5' ss). We show here, using specific NRS mutations to disrupt U11 binding and coexpression of U11snRNA genes harboring compensatory mutations, that the NRS U11 site is functional when paired with a minor-class 3' ss from the human P120 gene, Surprisingly, the expectation that the same NRS mutants would be defective for splicing inhibition proved false; splicing inhibition was as good as, if not better than, that for the wild-type NRS, Comparison of these new mutations with RG11 indicated that the latter may disrupt binding of a factor(s) other than U11. Our data suggest that this factor is U1 snRNP and that a U1 binding site that overlaps the U11 site is also disrupted by RG11, Analysis of mutations which selectively disrupted U1 or U11 binding indicated that splicing inhibition by the NRS correlates most strongly with U1 snRNP. Additionally, we show that U1 binding is facilitated by SR proteins that bind tothe 5' half of the NRS, confirming an earlier proposal that this region isinvolved in recruiting snRNPs to the NRS, These data indicate a functionalrole for U1 in NRS-mediated splicing inhibition.

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Documento generato il 27/10/20 alle ore 10:28:09