REVIEW PAPER
Regulation of alternative splicing by RNA secondary structure
Publication date: 2015-10-06
BioTechnologia 2014;95(3):181-186
KEYWORDS
ABSTRACT
The alternative splicing process is controlled by trans-acting factors and cis-acting elements. Initially, it was
thought that hnRNP proteins interact with the newly synthetized transcript and prevent the generation of a premRNA
secondary structure. However, there are many examples of the impact of secondary structure on the
alternative splicing of genes. An alternative splicing regulation is presented based on: the recognition of 5N and
3N splicing sites and branch sites, regulatory cis-acting elements, long-range interaction.
thought that hnRNP proteins interact with the newly synthetized transcript and prevent the generation of a premRNA
secondary structure. However, there are many examples of the impact of secondary structure on the
alternative splicing of genes. An alternative splicing regulation is presented based on: the recognition of 5N and
3N splicing sites and branch sites, regulatory cis-acting elements, long-range interaction.
REFERENCES (28)
1.
Baraniak A.P., Lasda E.L., Wagner E.J., Garcia-Blanco M.A.(2003) A stem structure in fibroblast growth factor receptor2 transcripts mediates cell-type-specific splicing by approximating intronic control elements. Mol. Cell Biol. 23:9327-9337.
2.
Barash Y., Calarco J.A., Gao W., Pan Q., Wang X., Shai O.,Blencowe B.J., Frey B.J. (2010) Deciphering the splicing code. Nature 465: 53-59.
3.
Blanchette M., Chabot B. (1997) A highly stable duplex structure sequesters the 5N splice site region of hnRNP A1 alternative exon 7B. RNA 3: 405-419.
4.
Buratti E., Baralle F.E. (2004) Influence of RNA secondary structure on the pre-mRNA splicing process. Mol. Cell Biol. 24: 10505-10514.
5.
Estes P.A., Cooke N.E., Liebhaber S.A. (1992) A native RNA secondary structure controls alternative splice-site selection, generates two human growth hormone isoforms.J. Biol. Chem. 267: 14902-14908.
6.
Graveley B.R. (2005) Mutually exclusive splicing of the insect Dscam pre-mRNA directed by competing intronic RNA secondary structures. Cell 123: 65-73.
7.
Hiller M., Zhang Z., Backofen R., Stamm S. (2007) Pre-mRNA secondary structures influence exon recognition. PLoS Genet 3: e204.
8.
Hutton M., Lendon C.L., Rizzu P., Baker M., Froelich S., Houlden H., Pickering-Brown S., Chakraverty S., Isaacs A., Grover A., et al. (1998) Association of missense andb5N-splice-site mutations in tau with the inherited dementia FTDP-17. Nature 393: 702-705.
9.
Iijima M., Tabira T., Poorkaj P., Schellenberg G.D., Trojanowski J.Q., Lee V.M., Schmidt M.L., Takahashi K., Nabika T., Matsumoto T. et al. (1999) A distinct familial presenile dementia with a novel missense mutation in the tau gene. Neuroreport 10: 497-501.
10.
Libri D., Stutz F., McCarthy T., Rosbash M. (1995) RNA structural patterns and splicing: molecular basis for an RNA-based enhancer. RNA 1: 425-436.
11.
Lisowiec J., Magner D., Kierzek E., Lenartowicz E., Kierzek R. (2015) Structural determinants for alternative splicing regulation of the MAPT pre-mRNA. RNA Biol. 12: 330-342.
12.
Maris C., Dominguez C., Allain F.H. (2005) The RNA recognition motif, a plastic RNA-binding platform to regulate posttranscriptional gene expression. FEBS J. 272: 2118-2131.
13.
Miyamoto K., Kowalska A., Hasegawa M., Tabira T., Takahashi K., Araki W., Akiguchi I., Ikemoto A. (2001) Familial frontotemporal dementia and parkinsonism with a novel mutation at an intron 10+11-splice site in the tau gene. Ann. Neurol. 50: 117-120.
14.
Monani U.R. (2005) Spinal muscular atrophy: a deficiency in a ubiquitous protein; a motor neuron-specific disease. Neuron 48: 885-896.
15.
Muro A.F., Caputi M., Pariyarath R., Pagani F., Buratti E., Baralle F.E. (1999) Regulation of fibronectin EDA exon alternative splicing: possible role of RNA secondary structure for enhancer display. Mol. Cell Biol. 19: 2657-2671.
16.
Pagani F., Raponi M., Baralle F.E. (2005) Synonymous mutations in CFTR exon 12 affect splicing and are not neutral in evolution. Proc. Natl. Acad. Sci. USA 102: 6368-6372.
17.
Shen L.X., Basilion J.P., Stanton V.P. Jr. (1999) Single-nucleotide polymorphisms can cause different structural folds of mRNA. Proc. Natl. Acad. Sci. USA 96: 7871-7876.
18.
Shepard P.J., Hertel K.J. (2008) Conserved RNA secondary structures promote alternative splicing. RNA 14: 1463-1469.
19.
Sirand-Pugnet P., Durosay P., Clouet d’Orval B.C., Brody E., Marie J. (1995) beta-Tropomyosin pre-mRNA folding around a muscle-specific exon interferes with several steps of spliceosome assembly. J. Mol. Biol. 251: 591-602.
20.
Stanford P.M., Halliday G.M., Brooks W.S., Kwok J.B., Storey C.E., Creasey H., Morris J. G., Fulham M.J., Schofield P.R.(2000) Progressive supranuclear palsy pathology caused by a novel silent mutation in exon 10 of the tau gene: expansion of the disease phenotype caused by tau gene mutations. Brain 123 (Pt. 5): 880-893.
21.
Stanford P.M., Shepherd C.E., Halliday G.M., Brooks W.S., Schofield P.W., Brodaty H., Martins R.N., Kwok J.B., Schofield P.R. (2003) Mutations in the tau gene that cause an increase in three repeat tau and frontotemporal dementia. Brain 126: 814-826.
22.
Tolnay M., Grazia Spillantini M., Rizzini C., Eccles D., Lowe J., Ellison D. (2000) A new case of frontotemporal dementia and parkinsonism resulting from an intron 10 +3-splice site mutation in the tau gene: clinical and pathological features. Neuropathol. Appl. Neurobiol. 26: 368-378.
23.
Varani L., Hasegawa M., Spillantini M.G., Smith M.J., Murrell J.R., Ghetti B., Klug A., Goedert M., Varani G. (1999) Structure of tau exon 10 splicing regulatory element RNA and destabilization by mutations of frontotemporal dementia and parkinsonism linked to chromosome 17. Proc. Natl. Acad. Sci. USA 96: 8229-8234.
25.
Understanding the transcriptome through RNA structure. Nat. Rev. Genet. 12: 641-655.
28.
Yasuda M., Takamatsu J., D’Souza I., Crowther R.A., Kawamata T., Hasegawa M., Hasegawa H., Spillantini M.G., Tanimukai S., Poorkaj P. et al. (2000) A novel mutation at position +12 in the intron following exon 10 of the tau gene in familial frontotemporal dementia (FTD-Kumamoto). Ann. Neurol. 47: 422-429.
Share
RELATED ARTICLE
| eISSN: | 2353-9461 |
| ISSN: | 0860-7796 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
