RNAi-mediated PTB depletion leads to enhanced exon definition

Eric J. Wagner; Mariano A. Garcia-Blanco

doi:10.1016/S1097-2765(02)00645-7

RNAi-mediated PTB depletion leads to enhanced exon definition

Eric J. Wagner, Mariano A. Garcia-Blanco

Research output: Contribution to journal › Article › peer-review

121 Scopus citations

Abstract

Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo.

Original language	English (US)
Pages (from-to)	943-949
Number of pages	7
Journal	Molecular cell
Volume	10
Issue number	4
DOIs	https://doi.org/10.1016/S1097-2765(02)00645-7
State	Published - Oct 1 2002
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1016/S1097-2765(02)00645-7

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title = "RNAi-mediated PTB depletion leads to enhanced exon definition",

abstract = "Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo.",

author = "Wagner, {Eric J.} and Garcia-Blanco, {Mariano A.}",

note = "Funding Information: We thank by B. Cullen and R. Carstens for contributing constructs and reagents. We thank A. Baraniak, A. Baines, J. Pearson, and N. Robson for critically reading this manuscript. We also acknowledge A. Kennett for outstanding administrative support. This work was supported by the NIH RO1 GM63090 grant to M.A.G.-B. who also acknowledges support from the Raymond and Beverly Sackler Foundation. E.J.W. acknowledges support of a DOD predoctoral fellowship.",

year = "2002",

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doi = "10.1016/S1097-2765(02)00645-7",

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journal = "Molecular cell",

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T1 - RNAi-mediated PTB depletion leads to enhanced exon definition

AU - Wagner, Eric J.

AU - Garcia-Blanco, Mariano A.

N1 - Funding Information: We thank by B. Cullen and R. Carstens for contributing constructs and reagents. We thank A. Baraniak, A. Baines, J. Pearson, and N. Robson for critically reading this manuscript. We also acknowledge A. Kennett for outstanding administrative support. This work was supported by the NIH RO1 GM63090 grant to M.A.G.-B. who also acknowledges support from the Raymond and Beverly Sackler Foundation. E.J.W. acknowledges support of a DOD predoctoral fellowship.

PY - 2002/10/1

Y1 - 2002/10/1

N2 - Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo.

AB - Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo.

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U2 - 10.1016/S1097-2765(02)00645-7

DO - 10.1016/S1097-2765(02)00645-7

M3 - Article

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AN - SCOPUS:0036810248

SN - 1097-2765

VL - 10

SP - 943

EP - 949

JO - Molecular cell

JF - Molecular cell

IS - 4

ER -

RNAi-mediated PTB depletion leads to enhanced exon definition

Abstract

ASJC Scopus subject areas

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