CUG-BP binds to RNA substrates and recruits PARN deadenylase

被引:142
作者
Moraes, Karen C. M. [1 ]
Wilusz, Carol J. [1 ]
Wilusz, Jeffrey [1 ]
机构
[1] Colorado State Univ, Coll Vet Med & Biomed Sci, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA
关键词
deadenylation; mRNA stability; myotonic dystrophy; EDEN; AU-rich;
D O I
10.1261/rna.59606
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
CUG-BP is the human homolog of the Xenopus EDEN-BP, which was shown previously to bind to mRNAs, such as c-mos, that exhibit rapid deadenylation following fertilization of the oocyte. While several studies have focused on roles of CUG-BP as a splicing or translation regulator in mammalian cells, its role in mRNA decay has not been examined in detail. Here, we have used an in vitro deadenylation assay to dissect the function of CUG-BP in the decay of two ARE-containing mRNAs: c-fos and TNF alpha. CUG-BP binds specifically to both of these RNAs and stimulates poly(A) shortening by PARN. Moreover, CUG-BP interacts with PARN in extracts by coimmunoprecipitation, and this interaction can be recapitulated using recombinant proteins. CUG-BP, therefore, is the first RNA-binding protein shown to directly recruit a deadenylase to an RNA substrate.
引用
收藏
页码:1084 / 1091
页数:8
相关论文
共 32 条
[21]   c-Jun ARE targets mRNA deadenylation by an EDEN-BP (embryo deadenylation element-binding protein)-dependent pathway [J].
Paillard, L ;
Legagneux, V ;
Maniey, D ;
Osborne, HB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (05) :3232-3235
[22]   EDEN and EDEN-BP, a cis element and an associated factor that mediate sequence-specific mRNA deadenylation in Xenopus embryos [J].
Paillard, L ;
Omilli, F ;
Legagneux, V ;
Bassez, T ;
Maniey, D ;
Osborne, HB .
EMBO JOURNAL, 1998, 17 (01) :278-287
[23]   Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy [J].
Philips, AV ;
Timchenko, LT ;
Cooper, TA .
SCIENCE, 1998, 280 (5364) :737-741
[24]   Cytoplasmic polyadenylation in development and beyond [J].
Richter, JD .
MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, 1999, 63 (02) :446-+
[25]   Altered phosphorylation and intracellular distribution of a (CUG)(n) triplet repeat RNA binding protein in patients with myotonic dystrophy and in myotonin protein kinase knockout mice [J].
Roberts, R ;
Timchenko, NA ;
Miller, JW ;
Reddy, S ;
Caskey, CT ;
Swanson, MS ;
Timchenko, LT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (24) :13221-13226
[26]   The CUG-binding protein binds specifically to UG dinucleotide repeats in a yeast three-hybrid system [J].
Takahashi, N ;
Sasagawa, N ;
Suzuki, K ;
Ishiura, S .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 277 (02) :518-523
[27]   Identification of a (CUG)(n) triplet repeat RNA-binding protein and its expression in myotonic dystrophy [J].
Timchenko, LT ;
Miller, JW ;
Timchenko, NA ;
DeVore, DR ;
Datar, KV ;
Lin, LJ ;
Roberts, R ;
Caskey, CT ;
Swanson, MS .
NUCLEIC ACIDS RESEARCH, 1996, 24 (22) :4407-4414
[28]   RNA CUG-binding protein 1 increases translation of 20-kDa isoform of CCAAT/enhancer-binding protein β by interacting with the α and β subunits of eukaryotic initiation translation factor 2 [J].
Timchenko, NA ;
Wang, GL ;
Timchenko, LT .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (21) :20549-20557
[29]   AUUUA sequences direct mRNA deadenylation uncoupled from decay during Xenopus early development [J].
Voeltz, GK ;
Steitz, JA .
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (12) :7537-7545
[30]   Bringing the role of rnRNA decay in the control of gene expression into focus [J].
Wilusz, CJ ;
Wilusz, J .
TRENDS IN GENETICS, 2004, 20 (10) :491-497