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Crossregulation and functional redundancy between the splicing regulator PTB and its paralogs nPTB and ROD1.
Mol Cell. 2007 Aug 03; 27(3):420-34.MC

Abstract

Among the targets of the repressive splicing regulator, polypyrimidine tract binding protein (PTB) is its own pre-mRNA, where PTB-induced exon 11 skipping produces an RNA substrate for nonsense-mediated decay (NMD). To identify additional PTB-regulated alternative splicing events, we used quantitative proteomic analysis of HeLa cells after knockdown of PTB. Apart from loss of PTB, the only change was upregulation of the neuronally restricted nPTB, resulting from decreased skipping of nPTB exon 10, a splicing event that leads to NMD of nPTB mRNA. Compared with knockdown of PTB alone, simultaneous knockdown of PTB and nPTB led to larger changes in alternative splicing of known and newly identified PTB-regulated splicing events. Strikingly, the hematopoietic PTB paralog ROD1 also switched from a nonproductive splicing pathway upon PTB/nPTB knockdown. Our data indicate crossregulation between PTB and its paralogs via nonproductive alternative splicing and a large degree of functional overlap between PTB and nPTB.

Authors+Show Affiliations

Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge, UK.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

17679092

Citation

Spellman, Rachel, et al. "Crossregulation and Functional Redundancy Between the Splicing Regulator PTB and Its Paralogs nPTB and ROD1." Molecular Cell, vol. 27, no. 3, 2007, pp. 420-34.
Spellman R, Llorian M, Smith CW. Crossregulation and functional redundancy between the splicing regulator PTB and its paralogs nPTB and ROD1. Mol Cell. 2007;27(3):420-34.
Spellman, R., Llorian, M., & Smith, C. W. (2007). Crossregulation and functional redundancy between the splicing regulator PTB and its paralogs nPTB and ROD1. Molecular Cell, 27(3), 420-34.
Spellman R, Llorian M, Smith CW. Crossregulation and Functional Redundancy Between the Splicing Regulator PTB and Its Paralogs nPTB and ROD1. Mol Cell. 2007 Aug 3;27(3):420-34. PubMed PMID: 17679092.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Crossregulation and functional redundancy between the splicing regulator PTB and its paralogs nPTB and ROD1. AU - Spellman,Rachel, AU - Llorian,Miriam, AU - Smith,Christopher W J, PY - 2006/12/19/received PY - 2007/05/11/revised PY - 2007/06/12/accepted PY - 2007/8/7/pubmed PY - 2007/8/28/medline PY - 2007/8/7/entrez SP - 420 EP - 34 JF - Molecular cell JO - Mol. Cell VL - 27 IS - 3 N2 - Among the targets of the repressive splicing regulator, polypyrimidine tract binding protein (PTB) is its own pre-mRNA, where PTB-induced exon 11 skipping produces an RNA substrate for nonsense-mediated decay (NMD). To identify additional PTB-regulated alternative splicing events, we used quantitative proteomic analysis of HeLa cells after knockdown of PTB. Apart from loss of PTB, the only change was upregulation of the neuronally restricted nPTB, resulting from decreased skipping of nPTB exon 10, a splicing event that leads to NMD of nPTB mRNA. Compared with knockdown of PTB alone, simultaneous knockdown of PTB and nPTB led to larger changes in alternative splicing of known and newly identified PTB-regulated splicing events. Strikingly, the hematopoietic PTB paralog ROD1 also switched from a nonproductive splicing pathway upon PTB/nPTB knockdown. Our data indicate crossregulation between PTB and its paralogs via nonproductive alternative splicing and a large degree of functional overlap between PTB and nPTB. SN - 1097-2765 UR - https://www.unboundmedicine.com/medline/citation/17679092/Crossregulation_and_functional_redundancy_between_the_splicing_regulator_PTB_and_its_paralogs_nPTB_and_ROD1_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1097-2765(07)00406-6 DB - PRIME DP - Unbound Medicine ER -