Literature DB >> 10496225

Dissecting FMR1, the protein responsible for fragile X syndrome, in its structural and functional domains.

S Adinolfi1, C Bagni, G Musco, T Gibson, L Mazzarella, A Pastore.   

Abstract

FMR1 is an RNA-binding protein that is either absent or mutated in patients affected by the fragile X syndrome, the most common inherited cause of mental retardation in humans. Sequence analysis of the FMR1 protein has suggested that RNA binding is related to the presence of two K-homologous (KH) modules and an RGG box. However, no attempt has been so far made to map the RNA-binding sites along the protein sequence and to identify possible differential RNA-sequence specificity. In the present article, we describe work done to dissect FMR1 into regions with structurally and functionally distinct properties. A semirational approach was followed to identify four regions: an N-terminal stretch of 200 amino acids, the two KH regions, and a C-terminal stretch. Each region was produced as a recombinant protein, purified, and probed for its state of folding by spectroscopical techniques. Circular dichroism and NMR spectra of the N-terminus show formation of secondary structure with a strong tendency to aggregate. Of the two homologous KH motifs, only the first one is folded whereas the second remains unfolded even when it is extended both N- and C-terminally. The C-terminus is, as expected from its amino acid composition, nonglobular. Binding assays were then performed using the 4-nt homopolymers. Our results show that only the first KH domain but not the second binds to RNA, and provide the first direct evidence for RNA binding of both the N-terminal and the C-terminal regions. RNA binding for the N-terminus could not be predicted from sequence analysis because no known RNA-binding motif is identifiable in this region. Different sequence specificity was observed for the fragments: both the N-terminus of the protein and KH1 bind preferentially to poly-(rG). The C-terminal region, which contains the RGG box, is nonspecific, as it recognizes the bases with comparable affinity. We therefore conclude that FMR1 is a protein with multiple sites of interaction with RNA: sequence specificity is most likely achieved by the whole block that comprises the first approximately 400 residues, whereas the C-terminus provides a nonspecific binding surface.

Entities:  

Mesh:

Substances:

Year:  1999        PMID: 10496225      PMCID: PMC1369847          DOI: 10.1017/s1355838299990647

Source DB:  PubMed          Journal:  RNA        ISSN: 1355-8382            Impact factor:   4.942


  37 in total

1.  The KH domain occurs in a diverse set of RNA-binding proteins that include the antiterminator NusA and is probably involved in binding to nucleic acid.

Authors:  T J Gibson; J D Thompson; J Heringa
Journal:  FEBS Lett       Date:  1993-06-21       Impact factor: 4.124

2.  Nucleus basalis magnocellularis and hippocampus are the major sites of FMR-1 expression in the human fetal brain.

Authors:  M Abitbol; C Menini; A L Delezoide; T Rhyner; M Vekemans; J Mallet
Journal:  Nat Genet       Date:  1993-06       Impact factor: 38.330

3.  Improved prediction of protein secondary structure by use of sequence profiles and neural networks.

Authors:  B Rost; C Sander
Journal:  Proc Natl Acad Sci U S A       Date:  1993-08-15       Impact factor: 11.205

4.  The FMR-1 protein is cytoplasmic, most abundant in neurons and appears normal in carriers of a fragile X premutation.

Authors:  D Devys; Y Lutz; N Rouyer; J P Bellocq; J L Mandel
Journal:  Nat Genet       Date:  1993-08       Impact factor: 38.330

5.  The pre-mRNA binding K protein contains a novel evolutionarily conserved motif.

Authors:  H Siomi; M J Matunis; W M Michael; G Dreyfuss
Journal:  Nucleic Acids Res       Date:  1993-03-11       Impact factor: 16.971

6.  Essential role for KH domains in RNA binding: impaired RNA binding by a mutation in the KH domain of FMR1 that causes fragile X syndrome.

Authors:  H Siomi; M Choi; M C Siomi; R L Nussbaum; G Dreyfuss
Journal:  Cell       Date:  1994-04-08       Impact factor: 41.582

7.  Characterisation of two major cellular poly(rC)-binding human proteins, each containing three K-homologous (KH) domains.

Authors:  H Leffers; K Dejgaard; J E Celis
Journal:  Eur J Biochem       Date:  1995-06-01

Review 8.  Molecular genetics of the fragile-X syndrome: a novel type of unstable mutation.

Authors:  J L Mandel; D Heitz
Journal:  Curr Opin Genet Dev       Date:  1992-06       Impact factor: 5.578

9.  Protein-rRNA binding features and their structural and functional implications in ribosomes as determined by cross-linking studies.

Authors:  H Urlaub; V Kruft; O Bischof; E C Müller; B Wittmann-Liebold
Journal:  EMBO J       Date:  1995-09-15       Impact factor: 11.598

10.  FXR1, an autosomal homolog of the fragile X mental retardation gene.

Authors:  M C Siomi; H Siomi; W H Sauer; S Srinivasan; R L Nussbaum; G Dreyfuss
Journal:  EMBO J       Date:  1995-06-01       Impact factor: 11.598

View more
  30 in total

Review 1.  Candidate RNA-binding proteins regulating extrasomatic mRNA targeting and translation in mammalian neurons.

Authors:  Stefan Kindler; Michaela Monshausen
Journal:  Mol Neurobiol       Date:  2002-04       Impact factor: 5.590

2.  The role of a clinically important mutation in the fold and RNA-binding properties of KH motifs.

Authors:  Andres Ramos; David Hollingworth; Annalisa Pastore
Journal:  RNA       Date:  2003-03       Impact factor: 4.942

3.  A highly conserved protein family interacting with the fragile X mental retardation protein (FMRP) and displaying selective interactions with FMRP-related proteins FXR1P and FXR2P.

Authors:  A Schenck; B Bardoni; A Moro; C Bagni; J L Mandel
Journal:  Proc Natl Acad Sci U S A       Date:  2001-07-03       Impact factor: 11.205

4.  Substitution of critical isoleucines in the KH domains of Drosophila fragile X protein results in partial loss-of-function phenotypes.

Authors:  Paromita Banerjee; Shweta Nayar; Sarita Hebbar; Catherine F Fox; Michele C Jacobs; Jae H Park; Joyce J Fernandes; Thomas C Dockendorff
Journal:  Genetics       Date:  2006-12-28       Impact factor: 4.562

Review 5.  Fragile X-associated disorders: a clinical overview.

Authors:  Anne Gallagher; Brian Hallahan
Journal:  J Neurol       Date:  2011-07-12       Impact factor: 4.849

6.  The fragile X mental retardation protein inhibits translation via interacting with mRNA.

Authors:  Z Li; Y Zhang; L Ku; K D Wilkinson; S T Warren; Y Feng
Journal:  Nucleic Acids Res       Date:  2001-06-01       Impact factor: 16.971

7.  The fragile X mental retardation protein and group I metabotropic glutamate receptors regulate levels of mRNA granules in brain.

Authors:  Armaz Aschrafi; Bruce A Cunningham; Gerald M Edelman; Peter W Vanderklish
Journal:  Proc Natl Acad Sci U S A       Date:  2005-01-31       Impact factor: 11.205

8.  RNAi-mediated depletion of the 15 KH domain protein, vigilin, induces death of dividing and non-dividing human cells but does not initially inhibit protein synthesis.

Authors:  Kathryn M Goolsby; David J Shapiro
Journal:  Nucleic Acids Res       Date:  2003-10-01       Impact factor: 16.971

Review 9.  Fragile X-related protein family: a double-edged sword in neurodevelopmental disorders and cancer.

Authors:  Mrinmoyee Majumder; Roger H Johnson; Viswanathan Palanisamy
Journal:  Crit Rev Biochem Mol Biol       Date:  2020-09-02       Impact factor: 8.250

10.  The HSV-1 ICP27 RGG box specifically binds flexible, GC-rich sequences but not G-quartet structures.

Authors:  Kara A Corbin-Lickfett; I-Hsiung Brandon Chen; Melanie J Cocco; Rozanne M Sandri-Goldin
Journal:  Nucleic Acids Res       Date:  2009-11       Impact factor: 16.971

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.