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Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins.
Mol Cell. 2001 Dec; 8(6):1351-61.MC

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.

Authors+Show Affiliations

Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

11779509

Citation

Zhu, J, et al. "Exon Identity Established Through Differential Antagonism Between Exonic Splicing Silencer-bound hnRNP A1 and Enhancer-bound SR Proteins." Molecular Cell, vol. 8, no. 6, 2001, pp. 1351-61.
Zhu J, Mayeda A, Krainer AR. Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins. Mol Cell. 2001;8(6):1351-61.
Zhu, J., Mayeda, A., & Krainer, A. R. (2001). Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins. Molecular Cell, 8(6), 1351-61.
Zhu J, Mayeda A, Krainer AR. Exon Identity Established Through Differential Antagonism Between Exonic Splicing Silencer-bound hnRNP A1 and Enhancer-bound SR Proteins. Mol Cell. 2001;8(6):1351-61. PubMed PMID: 11779509.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins. AU - Zhu,J, AU - Mayeda,A, AU - Krainer,A R, PY - 2002/1/10/pubmed PY - 2002/1/17/medline PY - 2002/1/10/entrez SP - 1351 EP - 61 JF - Molecular cell JO - Mol Cell VL - 8 IS - 6 N2 - 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. SN - 1097-2765 UR - https://www.unboundmedicine.com/medline/citation/11779509/Exon_identity_established_through_differential_antagonism_between_exonic_splicing_silencer_bound_hnRNP_A1_and_enhancer_bound_SR_proteins_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1097-2765(01)00409-9 DB - PRIME DP - Unbound Medicine ER -