SC35 and heterogeneous nuclear ribonucleoprotein A/B proteins bind to a juxtaposed exonic splicing enhancer/exonic splicing silencer element to regulate HIV-1 tat exon 2 splicing

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  • Alan M Zahler, Department of Molecular, Cellular and Developmental Biology and Center for Molecular Biology of RNA, Sinsheimer Laboratories, University of California, USA
  • Christian K Damgaard
  • Jørgen Kjems
  • Massimo Caputi, Biomedical Science Department, Florida Atlantic University, USA
Splicing of the human immunodeficiency virus, type 1, primary transcript is highly regulated. Maintaining the proper equilibrium among spliced, unspliced, and partially spliced isoforms is essential for the replication of the virus. Here we characterize a complex cis-acting element located in tat exon 2 that is required for the splicing regulation of the upstream intron. An exonic splicing enhancer (ESE) and an exonic splicing silencer (ESS) are both located within the regulatory element. Heterogeneous nuclear ribonucleoprotein (hnRNP) A/B proteins bind the ESS to repress splicing, whereas the SR protein SC35 binds the ESE to activate it. We show that the SC35 and the hnRNP A1 binding sites overlap within the juxtaposed ESE/ESS. We propose that hnRNP A1 binding to the ESS inhibits splicing of the upstream intron by directly masking the SC35 binding site.
OriginalsprogEngelsk
TidsskriftJournal of Biological Chemistry
Vol/bind279
Nummer11
Sider (fra-til)10077-10084
Antal sider8
ISSN0021-9258
DOI
StatusUdgivet - 12 mar. 2004

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