Zhu, J., Mayeda, A., Krainer, A. R. (December 2001) Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins. Molecular Cell, 8 (6). pp. 1351-1361. ISSN 1097-2765
Abstract
SR proteins recognize exonic splicing enhancer (ESE) elements and promote exon use, whereas certain hnRNP proteins bind to exonic splicing silencer (ESS) elements and block exon recognition. We investigated how ESS3 in HIV-1 tat exon 3 blocks splicing promoted by one SR protein (SC35) but not another (SF2/ASF). hnRNP A1 mediates silencing by binding initially to a required high-affinity site in ESS3, which then promotes further hnRNP A1 association with the upstream region of the exon. Both SC35 and SF2/ASF recognize upstream ESE motifs, but only SF2/ASF prevents secondary hnRNP A1 binding, presumably by blocking its cooperative propagation along the exon. The differential antagonism between a negative and two positive regulators exemplifies how inclusion of an alternative exon can be modulated.
| Item Type: | Paper |
|---|---|
| Uncontrolled Keywords: | pre-messenger-rna immunodeficiency-virus type-1 heterogeneous nuclear ribonucleoprotein a/b proteins cooperative binding rs domain tat exon in-vivo expression mechanism |
| Subjects: | bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > exons > exon splicing bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > nuclear ribonucleoprotein |
| CSHL Authors: | |
| Communities: | CSHL labs > Krainer lab |
| Depositing User: | Matt Covey |
| Date: | December 2001 |
| Date Deposited: | 11 Dec 2013 20:41 |
| Last Modified: | 11 Dec 2013 20:41 |
| Related URLs: | |
| URI: | https://repository.cshl.edu/id/eprint/28906 |
Actions (login required)
 |
Administrator's edit/view item |