抄録
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.
本文言語 | 英語 |
---|---|
ページ(範囲) | 1351-1361 |
ページ数 | 11 |
ジャーナル | Molecular Cell |
巻 | 8 |
号 | 6 |
DOI | |
出版ステータス | 出版済み - 2001 |
外部発表 | はい |
All Science Journal Classification (ASJC) codes
- 分子生物学
- 細胞生物学