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SF2/ASF binds to a splicing enhancer in the third HIV-1 tat exon and stimulates U2AF binding independently of the RS domain.
J Mol Biol. 2001 Sep 28; 312(4):649-62.JM

Abstract

Splicing of a single HIV-1 primary transcript into more than 30 different mRNAs is regulated by a combination of suboptimal splice sites, cis-acting RNA splicing enhancers and silencers, and trans-acting factors. We have studied the splicing of the second tat intron (SD4 to SA7) and find that activation of splicing by SF2/ASF is mediated by a degenerate exon splicing enhancer (ESE3), consisting of at least three functionally independent sub-elements. One of these sub-elements appears to have both enhancing and silencing properties, depending on the context. SF2/ASF stimulates U2AF65 binding to the suboptimal tat polypyrimidine tract in an ESE3-dependent manner, whereas the exon splicing silencer (ESS3) that is located downstream of the ESE3 inhibits this step. Truncated SF2/ASF protein without the RS domain binds specifically to the ESE3 and retains almost full capacity to stimulate U2AF65 binding and activate splicing. This suggests that SF2/ASF can stimulate the recruitment of U2AF65 by an RS domain-independent mechanism.

Authors+Show Affiliations

Department of Molecular and Structural Biology, University of Aarhus, C.F. Møllers Allé Building 130, DK-8000 Arhus C, Denmark.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11575921

Citation

Tange, T Ø, and J Kjems. "SF2/ASF Binds to a Splicing Enhancer in the Third HIV-1 Tat Exon and Stimulates U2AF Binding Independently of the RS Domain." Journal of Molecular Biology, vol. 312, no. 4, 2001, pp. 649-62.
Tange TØ, Kjems J. SF2/ASF binds to a splicing enhancer in the third HIV-1 tat exon and stimulates U2AF binding independently of the RS domain. J Mol Biol. 2001;312(4):649-62.
Tange, T. Ø., & Kjems, J. (2001). SF2/ASF binds to a splicing enhancer in the third HIV-1 tat exon and stimulates U2AF binding independently of the RS domain. Journal of Molecular Biology, 312(4), 649-62.
Tange TØ, Kjems J. SF2/ASF Binds to a Splicing Enhancer in the Third HIV-1 Tat Exon and Stimulates U2AF Binding Independently of the RS Domain. J Mol Biol. 2001 Sep 28;312(4):649-62. PubMed PMID: 11575921.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - SF2/ASF binds to a splicing enhancer in the third HIV-1 tat exon and stimulates U2AF binding independently of the RS domain. AU - Tange,T Ø, AU - Kjems,J, PY - 2001/9/29/pubmed PY - 2001/10/26/medline PY - 2001/9/29/entrez SP - 649 EP - 62 JF - Journal of molecular biology JO - J Mol Biol VL - 312 IS - 4 N2 - Splicing of a single HIV-1 primary transcript into more than 30 different mRNAs is regulated by a combination of suboptimal splice sites, cis-acting RNA splicing enhancers and silencers, and trans-acting factors. We have studied the splicing of the second tat intron (SD4 to SA7) and find that activation of splicing by SF2/ASF is mediated by a degenerate exon splicing enhancer (ESE3), consisting of at least three functionally independent sub-elements. One of these sub-elements appears to have both enhancing and silencing properties, depending on the context. SF2/ASF stimulates U2AF65 binding to the suboptimal tat polypyrimidine tract in an ESE3-dependent manner, whereas the exon splicing silencer (ESS3) that is located downstream of the ESE3 inhibits this step. Truncated SF2/ASF protein without the RS domain binds specifically to the ESE3 and retains almost full capacity to stimulate U2AF65 binding and activate splicing. This suggests that SF2/ASF can stimulate the recruitment of U2AF65 by an RS domain-independent mechanism. SN - 0022-2836 UR - https://www.unboundmedicine.com/medline/citation/11575921/SF2/ASF_binds_to_a_splicing_enhancer_in_the_third_HIV_1_tat_exon_and_stimulates_U2AF_binding_independently_of_the_RS_domain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2836(01)94971-X DB - PRIME DP - Unbound Medicine ER -