123
Views
300
CrossRef citations to date
0
Altmetric
Gene Expression

The CELF Family of RNA Binding Proteins Is Implicated in Cell-Specific and Developmentally Regulated Alternative Splicing

, &
Pages 1285-1296 | Received 13 Sep 2000, Accepted 09 Nov 2000, Published online: 28 Mar 2023

REFERENCES

  • Black, D. L.. 1992. Activation of c-src neuron-specific splicing by an unusual RNA element in vivo and in vitro. Cell 69:795–807.
  • Brook, J. D., M. E. McCurrach, H. G. Harley, A. J. Buckler, D. Church, H. Aburatani, K. Hunter, V. P. Stanton, J. P. Thirion, T. Hudson, R. Sohn, B. Zemelman, R. G. Snell, S. A. Rundle, S. Crow, J. Davies, P. Shelbourne, J. Buxton, C. Jones, V. Juvonen, K. Johnson, P. S. Harper, D. J. Shaw, and D. E. Housman. 1992. Molecular basis of myotonic dystrophy—expansion of a trinucleotide (CTG) repeat at the 3′ end of a transcript encoding a protein kinase family member. Cell 68:799–808.
  • Buckanovich, R. J., and R. B. Darnell. 1997. The neuronal RNA binding protein Nova-1 recognizes specific RNA targets in vitro and in vivo. Mol. Cell. Biol. 17:3194–3201.
  • Buckanovich, R. J., J. B. Posner, and R. B. Darnell. 1993. Nova, the paraneoplastic Ri antigen, is homologous to an RNA-binding protein and is specifically expressed in the developing motor system. Neuron 11:657–672.
  • Burd, C. G., and G. Dreyfuss. 1994. Conserved structures and diversity of functions of RNA-binding proteins. Science 265:615–621.
  • Cáceres, J. F., G. R. Screaton, and A. R. Krainer. 1998. A specific subset of SR proteins shuttles continuously between the nucleus and the cytoplasm. Genes Dev. 12:55–66.
  • Choi, D. K., T. Ito, Y. Mitsui, and Y. Sakaki. 1998. Fluorescent differential display analysis of gene expression in apoptotic neuroblastoma cells. Gene 223:21–31.
  • Chomczynski, P., and N. Sacchi. 1987. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal. Biochem. 162:156–159.
  • Cooper, T. A.. 1992. In vitro splicing of cardiac troponin T precursors. Exon mutations disrupt splicing of the upstream intron. J. Biol. Chem. 267:5330–5338.
  • Cooper, T. A.. 1998. Muscle-specific splicing of a heterologous exon mediated by a single muscle-specific splicing enhancer from the cardiac troponin T gene. Mol. Cell. Biol. 18:4519–4525.
  • Cooper, T. A., and C. P. Ordahl. 1985. A single cardiac troponin T gene generates embryonic and adult isoforms via developmentally regulated alternate splicing. J. Biol. Chem. 260:11140–11148.
  • Davis, B. M., M. E. McCurrach, K. L. Taneja, R. H. Singer, and D. E. Housman. 1997. Expansion of a CUG trinucleotide repeat in the 3′ untranslated region of myotonic dystrophy protein kinase transcripts results in nuclear retention of transcripts. Proc. Natl. Acad. Sci. USA 94:7388–7393.
  • Dignam, J. D., R. M. Lebovitz, and R. G. Roeder. 1983. Accurate transcription initiation by RNA polymerase II in a soluble extract from isolated mammalian nuclei. Nucleic Acids Res. 11:1475–1489.
  • Fu, X. D.. 1995. The superfamily of arginine/serine-rich splicing factors. RNA 1:663–680.
  • Fu, Y. H., A. Pizzuti, R. G. Fenwick, J. King, S. Rajnarayan, P. W. Dunne, J. Dubel, G. A. Nasser, T. Ashizawa, P. Dejong, B. Wieringa, R. Korneluk, M. B. Perryman, H. F. Epstein, and C. T. Caskey. 1992. An unstable triplet repeat in a gene related to myotonic muscular dystrophy. Science 255:1256–1258.
  • Godt, R. E., R. T. H. Fogaca, I. K. Silva, and T. M. Nosek. 1993. Contraction of developing avian heart muscle. Comp. Biochem. Physiol. [A] 105:213–218.
  • Good, P. J., Q. Chen, S. J. Warner, and D. Herring. 2000. A family of human RNA-binding proteins related to the Drosophila Bruno translational regulator. J. Biol. Chem. 275:28583–28592.
  • Gooding, C., G. C. Roberts, G. Moreau, B. Nadal-Ginard, and C. W. Smith. 1994. Smooth muscle-specific switching of alpha-tropomyosin mutually exclusive exon selection by specific inhibition of the strong default exon. EMBO J. 13:3861–3872.
  • Guo, W., G. J. Mulligan, S. Wormsley, and D. M. Helfman. 1991. Alternative splicing of beta-tropomyosin pre-mRNA: cis-acting elements and cellular factors that block the use of a skeletal muscle exon in nonmuscle cells. Genes Dev. 5:2096–2107.
  • Hanamura, A., J. F. Caceres, A. Mayeda, B. R. Franza Jr., and A. R. Krainer. 1998. Regulated tissue-specific expression of antagonistic pre-mRNA splicing factors. RNA 4:430–444.
  • Hanke, J., D. Brett, I. Zastrow, A. Aydin, S. Delbruck, G. Lehmann, F. Luft, J. Reich, and P. Bork. 1999. Alternative splicing of human genes: more the rule than the exception?. Trends Genet. 15:389–390.
  • Harper, P. S.. 1998. Myotonic dystrophy as a trinucleotide repeat disorder—a clinical perspective. Genetic instabilities and hereditary neurological diseases.. R. D. Wells, and S. T. Warren. 115–130. Academic Press, Boston, Mass
  • Higgins, D. G., and P. M. Sharp. 1989. Fast and sensitive multiple sequence alignments on a microcomputer. Comput. Appl. Biosci. 5:151–153.
  • Hofmann, K., P. Bucher, L. Falquet, and A. Bairoch. 1999. The PROSITE database, its status in 1999. Nuceic Acids Res. 27:215–219.
  • Hwang, D. M., W. S. Hwang, and C. C. Liew. 1994. Single pass sequencing of a unidirectional human fetal heart cDNA library to discover novel genes of the cardiovascular system. J. Mol. Cell Card 26:1329–1333.
  • Ichida, M., H. Endo, U. Ikeda, C. Matsuda, E. Ueno, K. Shimada, and Y. Kagawa. 1998. MyoD is indispensable for muscle-specific alternative splicing in mouse mitochondrial ATP synthase gamma-subunit pre-mRNA. J. Biol. Chem. 273:8492–8501.
  • Jensen, K. B., B. K. Dredge, G. Stefani, R. Zhong, R. J. Buckanovich, H. J. Okano, Y. Y. Yang, and R. B. Darnell. 2000. Nova-1 regulates neuron-specific alternative splicing and is essential for neuronal viability. Neuron 25:359–371.
  • Jin, J. P., and J. J. Lin. 1989. Isolation and characterization of cDNA clones encoding embryonic and adult isoforms of rat cardiac troponin T. J. Biol. Chem. 264:14471–14477.
  • Kaminski, A., S. L. Hunt, J. G. Patton, and R. J. Jackson. 1995. Direct evidence that polypyrimidine tract binding protein (PTB) is essential for internal initiation of translation of encepthalomyocarditis virus RNA. RNA 1:924–938.
  • Kamma, H., D. S. Portman, and G. Dreyfuss. 1995. Cell type-specific expression of hnRNP proteins. Exp. Cell Res. 221:187–196.
  • Kanopka, A., O. Muhlemann, S. Petersen-Mahrt, C. Estmer, C. Ohrmalm, and G. Akusjarvi. 1998. Regulation of adenovirus alternative RNA splicing by dephosphorylation of SR proteins. Nature 393:185–187.
  • Keene, J. D.. 1999. Why is Hu where? Shuttling of early-response-gene messenger RNA subsets. Proc. Natl. Acad. Sci. USA 96:5–7.
  • Kim-Ha, J., K. Kerr, and P. M. Macdonald. 1995. Translational regulation of oskar mRNA by bruno, an ovarian RNA-binding protein, is essential. Cell 81:403–412.
  • Lin, C. H., and J. G. Patton. 1995. Regulation of alternative 3′ splice site selection by constitutive splicing factors. RNA 1:234–245.
  • Lopez, A. J.. 1998. Alternative splicing of pre-mRNA: developmental consequences and mechanisms of regulation. Annu. Rev. Genet. 32:279–305.
  • Lu, X., N. A. Timchenko, and L. T. Timchenko. 1999. Cardiac elav-type RNA-binding protein (ETR-3) binds to RNA CUG repeats expanded in myotonic dystrophy. Hum. Mol. Genet. 8:53–60.
  • Mahadevan, M., C. Tsilfidis, L. Sabourin, G. Shutler, C. Amemiya, G. Jansen, C. Neville, M. Narang, J. Barcelo, K. Ohoy, S. Leblond, J. Earlemacdonald, P. J. Dejong, B. Wieringa, and R. G. Korneluk. 1992. Myotonic dystrophy mutation—an unstable CTG repeat in the 3′ untranslated region of the gene. Science 255:1253–1255.
  • Margolis, R. L., M. R. Abraham, S. B. Gatchell, S. H. Li, A. S. Kidwai, T. S. Breschel, O. C. Stine, C. Callahan, M. G. McInnis, and C. A. Ross. 1997. cDNAs with long CAG trinucleotide repeats from human brain. Hum. Genet. 100:114–122.
  • McAuliffe, J. J.. 1994. Delineation of the cardiac troponin T expression pattern during murine development. J. Cell. Biochem. 18 (Suppl.):W347
  • McAuliffe, J. J., L. Z. Gao, and R. J. Solaro. 1990. Changes in myofibrillar activation and troponin C Ca2+ binding associated with troponin T isoform switching in developing rabbit heart. Circ. Res. 66:1204–1216.
  • Miller, J. W., C. R. Urbinati, P. Teng-Umnuay, M. G. Stenberg, B. J. Byrne, C. A. Thornton, and M. S. Swanson. 2000. Recruitment of human muscleblind proteins to (CUG)n expansions associated with myotonic dystrophy. EMBO J. 19:4439–4448.
  • Milne, C. A., and J. Hodgkin. 1999. ETR-1, a homologue of a protein linked to myotonic dystropy, is essential for muscle development in Caenorhabditis elegans. Curr. Biol. 9:1243–1246.
  • Min, H., C. W. Turck, J. M. Nikolic, and D. L. Black. 1997. A new regulatory protein, KSRP, mediates exon inclusion through an intronic splicing enhancer. Genes Dev. 11:1023–1036.
  • Nakai, K., and M. Kanehisa. 1992. A knowledge base for predicting protein localization sites in eukaryotic cells. Genomics 14:897–911.
  • Paillard, L., F. Omilli, V. Legagneux, T. Bassez, D. Maniey, and H. B. Osborne. 1998. EDEN and EDEN-BP, a cis element and an associated factor that mediate sequence-specific mRNA deadenylation in Xenopus embryos. EMBO J. 17:278–287.
  • Philips, A. V., L. T. Timchenko, and T. A. Cooper. 1998. Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy. Science 280:737–741.
  • Piñol-Roma, S., and G. Dreyfuss. 1992. Shuttling of pre-mRNA binding proteins between nucleus and cytoplasm. Nature 355:730–732.
  • Polydorides, A. D., H. J. Okano, Y. Y. Yang, G. Stefani, and R. B. Darnell. 2000. A brain-enriched polypyrimidine tract-binding protein antagonizes the ability of Nova to regulate neuron-specific alternative splicing. Proc. Natl. Acad. Sci. USA 97:6350–6355.
  • Roberts, R., N. A. Timchenko, J. W. Miller, S. Reddy, C. T. Caskey, M. S. Swanson, and L. T. Timchenko. 1997. 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. Proc. Natl. Acad. Sci. USA 94:13221–13226.
  • Ryan, K. J., and T. A. Cooper. 1996. Muscle-specific splicing enhancers regulate inclusion of the cardiac troponin T alternative exon in embryonic skeletal muscle. Mol. Cell. Biol. 16:4014–4023.
  • Sabourin, L. A., K. Tamai, M. A. Narang, and R. G. Korneluk. 1997. Overexpression of 3′-untranslated region of the myotonic dystrophy kinase cDNA inhibits myoblast differentiation in vitro. J. Biol. Chem. 272:29626–29635.
  • Saitoh, O., E. N. Olson, and M. Periasamy. 1990. Muscle-specific RNA processing continues in the absence of myogenin expression. J. Biol. Chem. 265:19381–19384.
  • Sambrook, J., E. F. Fritsch, and T. Maniatis. 1989. Molecular cloning: a laboratory manual, 2nd ed. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y
  • Sanford, J. R., and J. P. Bruzik. 1999. Developmental regulation of SR protein phosphorylation and activity. Genes Dev. 13:1513–1518.
  • Sarnat, H. B., and S. W. Silbert. 1976. Maturational arrest of fetal muscle in neonatal myotonic dystrophy. A pathologic study of four cases. Arch. Neurol. 33:466–474.
  • Schultz, J., F. Milpetz, P. Bork, and C. P. Ponting. 1998. SMART, a simple modular architecture research tool: identification of signalling domains. Proc. Natl. Acad. Sci. USA 95:5857–5864.
  • Screaton, G. R., J. F. Caceres, A. Mayeda, M. V. Bell, M. Plebanski, D. G. Jackson, J. I. Bell, and A. R. Krainer. 1995. Identification and characterization of three members of the human SR family of pre-mRNA splicing factors. EMBO J. 14:4336–4349.
  • Singh, R., J. Valcarcel, and M. R. Green. 1995. Distinct binding specificities and functions of higher eukaryotic polypyrimidine tract-binding proteins. Science 268:1173–1176.
  • Timchenko, L. T., J. W. Miller, N. A. Timchenko, D. R. Devore, K. V. Datar, L. J. Lin, R. Roberts, C. T. Caskey, and M. S. Swanson. 1996. Identification of a (CUG)n triplet repeat RNA-binding protein and its expression in myotonic dystrophy. Nucleic Acids Res. 24:4407–4414.
  • Townsend, P. J., P. J. R. Barton, M. H. Yacoub, and H. Farza. 1995. Molecular cloning of human cardiac troponin T isoforms: expression in developing and failing heart. J. Mol. Cell Card 27:2223–2236.
  • Usuki, F., S. Ishiura, N. Saitoh, N. Sasagawa, H. Sorimachi, H. Kuzume, K. Maruyama, T. Terao, and K. Suzuki. 1997. Expanded CTG repeats in myotonin protein kinase suppresses myogenic differentiation. Neuroreport 8:3749–3753.
  • Wang, J., E. Pegoraro, E. Menegazzo, M. Gennarelli, R. C. Hoop, C. Angelini, and E. P. Hoffman. 1995. Myotonic dystrophy: evidence for a possible dominant-negative RNA mutation. Hum. Mol. Genet. 4:599–606.
  • Xie, W. Q., and L. I. Rothblum. 1991. Rapid, small-scale RNA isolation from tissue culture cells. BioTechniques 11:324–327.
  • Xu, R., J. Teng, and T. A. Cooper. 1993. The cardiac troponin T alternative exon contains a novel purine-rich positive splicing element. Mol. Cell. Biol. 13:3660–3674.
  • Zahler, A. M., K. M. Neugebauer, W. S. Lane, and M. B. Roth. 1993. Distinct functions of SR proteins in alternative pre-mRNA splicing. Science 260:219–222.
  • Zhang, L., M. Askiya, T. G. Sherman, and P. J. Grabowski. 1996. Essential nucleotides direct neuron-specific splicing of gamma-2 pre-mRNA. RNA 2:682–698.
  • Zhang, L., W. Liu, and P. J. Grabowski. 1999. Coordinate repression of a trio of neuron-specific splicing events by the splicing regulator PTB. RNA 5:117–130.
  • Zhang, W.-J., and J. Y. Wu. 1996. Functional properties of p54, a novel SR protein active in constitutive and alternative splicing. Mol. Cell. Biol. 16:5400–5408.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.