Navegar

Colección

Datos Estadísticas

Artículo

Nogués, G.; Kadener, S.; Cramer, P.; Bentley, D.; Kornblihtt, A.R. "Transcriptional activators differ in their abilities to control alternative splicing" (2002) Journal of Biological Chemistry. 277(45):43110-43114
Estamos trabajando para incorporar este artículo al repositorio
Consulte el artículo en la página del editor
Consulte la política de Acceso Abierto del editor

Abstract:

Promoter and enhancer elements can influence alter. native splicing, but the basis for this phenomenon is not well understood. Here we investigated how different transcriptional activators affect the decision between inclusion and exclusion (skipping) of the fibronectin EDI exon. A mutant of the acidic VP16 activation domain called SW6 that preferentially inhibits polymerase II (pol II) elongation caused a reduction in EDI exon skipping. Exon skipping was fully restored in the presence of the SW6 mutant by either the SV40 enhancer in cis or the human immunodeficiency virus (HIV) Tat in trans, both of which specifically stimulate pol II elongation. HIV Tat also cooperated with the Spl and CTF activation domains to enhance transcript elongation and EDI skipping. The extent of exon skipping correlated with the efficiency with which pol II transcripts reach the 3′ end of the gene but not with the overall fold increase in transcript levels caused by different activators. The ability of activators to enhance elongation by RNA polymerase II therefore correlates with their ability to enhance exon skipping. Consistent with this observation, the elongation inhibitor dichlororibofurano-sylbenzimldazole (DRB) enhanced EDI inclusion. Conversely, the histone deacetylase inhibitor trichostatin A that is thought to stimulate elongation caused a modest inhibition of EDI inclusion. Together our results support a kinetic coupling model in which the rate of transcript elongation determines the outcome of two competing splicing reactions that occur co-transcriptionally. Rapid, highly processive transcription favors EDI exon skipping, whereas slower, less processive transcription favors inclusion.

Registro:

Documento: Artículo
Título:Transcriptional activators differ in their abilities to control alternative splicing
Autor:Nogués, G.; Kadener, S.; Cramer, P.; Bentley, D.; Kornblihtt, A.R.
Filiación:Laboratorio de Fisiología y Biología Molecular, Departamento de Fisiología, Biología Molecular y Celular, Ciudad Universitaria, Pabellón II, C1428EHA Buenos Aires, Argentina
Department of Biochemistry and Molecular Genetics, University of Colorado Health Sciences Center, Denver, CO 80262, United States
Dept. of Molecular and Cellular Biology, Harvard University, 7 Divinity Ave, Cambridge, MA 02138, United States
Palabras clave:Enzyme inhibition; Enzymes; Genes; RNA; Viruses; Transcriptional activators; Biochemistry; 5,6 dichlorobenzimidazole riboside; fibronectin; histone deacetylase inhibitor; mutant protein; transactivator protein; transcription factor Sp1; trichostatin A; alternative RNA splicing; animal cell; article; correlation analysis; enhancer region; exon; nonhuman; priority journal; promoter region; protein domain; protein folding; Alternative Splicing; Animals; Antigens, Polyomavirus Transforming; Cercopithecus aethiops; COS Cells; Enhancer Elements (Genetics); Exons; Fibronectins; Gene Expression Regulation, Viral; Replication Origin; RNA Polymerase II; Simian virus 40; Trans-Activators; Transcription, Genetic; Transfection; Animalia; Human immunodeficiency virus
Año:2002
Volumen:277
Número:45
Página de inicio:43110
Página de fin:43114
DOI: http://dx.doi.org/10.1074/jbc.M208418200
Título revista:Journal of Biological Chemistry
Título revista abreviado:J. Biol. Chem.
ISSN:00219258
CODEN:JBCHA
CAS:Antigens, Polyomavirus Transforming; Fibronectins; RNA Polymerase II, EC 2.7.7.-; Trans-Activators
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v277_n45_p43110_Nogues

Referencias:

  • Bentley, D., (2002) Curr. Opin. Cell Biol., 14, pp. 336-342
  • Travers, A., (1999) Proc. Natl. Acad. Sci. U. S. A., 96, pp. 13634-13637
  • Maniatis, T., Reed, R., (2002) Nature, 416, pp. 499-506
  • Proudfoot, N.J., Furger, A., Dye, M.J., (2002) Cell, 108, pp. 501-512
  • Cáceres, J.F., Kornblihtt, A.R., (2002) Trends Genet., 18, pp. 186-193
  • McCracken, S., Fong, N., Rosonina, E., Yankulov, K., Brothers, G., Siderovski, D., Hessel, A., Bentley, D.L., (1997) Genes Dev., 11, pp. 3306-3318
  • McCracken, S., Fong, N., Yankulov, K., Ballantyne, S., Pan, G., Greenblatt, J., Patterson, S.D., Bentley, D., (1997) Nature, 385, pp. 357-361
  • Schroeder, S., Schwer, B., Shuman, S., Bentley, D., (2000) Genes Dev., 14, pp. 2435-2440
  • Komamitsky, P., Cho, E.J., Buratowski, S., (2000) Genes Dev., 14, pp. 2452-2460
  • Licatalosi, D.D., Geiger, G., Minet, M., Schroeder, S., Cilli, K., McNeil, J.B., Bentley, D.L., (2002) Mol. Cell, 9, pp. 1101-1111
  • Cramer, P., Pesce, C.G., Baralle, F.E., Kornblihtt, A.R., (1997) Proc. Natl. Acad. Sci. U. S. A., 94, pp. 11456-11460
  • Caputi, M., Casari, G., Guenzi, S., Tagliabue, R., Sidoli, A., Melo, C.A., Baralle, F.E., (1994) Nucleic Acids Res., 22, pp. 1018-1022
  • Cramer, P., Cáceres, J.F., Cazalla, D., Kadener, S., Muro, A.F., Baralle, F.E., Kornblihtt, A.R., (1999) Mol. Cell, 4, pp. 251-258
  • Kadener, S., Fededa, J.P., Rosbash, M., Kornblihtt, A.R., (2002) Proc. Natl. Acad. Sci. U. S. A., 99, pp. 8185-8190
  • Kadener, S., Cramer, P., Nogués, G., Cazalla, D., De la Mata, M., Fededa, J.P., Werbajh, S., Kornblihtt, A.R., (2001) EMBO J., 20, pp. 5759-5768
  • Yankulov, K., Blau, J., Purton, T., Roberts, S., Bentley, D.L., (1994) Cell, 77, pp. 749-759
  • Blau, J., Xiao, H., McCracken, S., O'Hare, P., Greenblatt, J., Bentley, D., (1996) Mol. Cell. Biol., 16, pp. 2044-2055
  • Kao, S.Y., Calman, A.F., Luciw, P.A., Peterlin, B.M., (1987) Nature, 330, pp. 489-493
  • Marciniak, R.A., Sharp, P.A., (1991) EMBO J., 10, pp. 4189-4196
  • Chomczynski, P., Sacchi, N., (1987) Anal. Biochem., 162, pp. 156-159
  • Walker, S., Greaves, R., O'Hare, P., (1993) Mol. Cell. Biol., 13, pp. 5233-5244
  • Nahreini, P., Mathews, M.B., (1995) J. Virol., 69, pp. 1296-1301
  • Mancebo, H.S., Lee, G., Flygare, J., Tomassini, J., Luu, P., Zhu, Y., Peng, J., Flores, O., (1997) Genes Dev., 11, pp. 2633-2644
  • Price, D.H., (2000) Mol. Cell. Biol., 20, pp. 2629-3634
  • Chodosh, L.A., Fire, A., Samuels, M., Sharp, P.A., (1989) J. Biol. Chem., 264, pp. 2250-2257
  • Madisen, L., Krumm, A., Hebbes, T.R., Groudine, M., (1998) Mol. Cell. Biol., 18, pp. 6281-6292
  • Vignali, M., Steger, D.J., Neely, K.E., Workman, J.L., (2000) EMBO J., 19, pp. 2629-2640
  • Lai, M.C., Teh, B.H., Tarn, W.Y., (1999) J. Biol. Chem., 274, pp. 11832-11841
  • Monsalve, M., Wu, Z., Adelmant, G., Puigserver, P., Fan, M., Spiegelman, B.M., (2000) Mol. Cell, 6, pp. 307-316
  • Zhou, Q., Sharp, P.A., (1996) Science, 274, pp. 605-610
  • Parada, C.A., Roeder, R.G., (1999) EMBO J., 18, pp. 3688-3701
  • Fong, Y.W., Zhou, Q., (2002) Nature, 414, pp. 929-933
  • Wittschieben, B., Otero, G., De Bizemont, T., Fellows, J., Erdjument-Bromage, H., Ohba, R., Li, Y., Svejstrup, J.Q., (1999) Mol. Cell, 4, pp. 123-128
  • Eperon, L.P., Graham, I.R., Griffiths, A.D., Eperon, I.C., (1988) Cell, 54, pp. 393-401
  • Roberts, G.C., Gooding, C., Mak, H.Y., Proudfoot, N.J., Smith, C.W.J., (1998) Nucleic Acids Res., 26, pp. 5568-5572

Citas:

---------- APA ----------
Nogués, G., Kadener, S., Cramer, P., Bentley, D. & Kornblihtt, A.R. (2002) . Transcriptional activators differ in their abilities to control alternative splicing. Journal of Biological Chemistry, 277(45), 43110-43114.
http://dx.doi.org/10.1074/jbc.M208418200
---------- CHICAGO ----------
Nogués, G., Kadener, S., Cramer, P., Bentley, D., Kornblihtt, A.R. "Transcriptional activators differ in their abilities to control alternative splicing" . Journal of Biological Chemistry 277, no. 45 (2002) : 43110-43114.
http://dx.doi.org/10.1074/jbc.M208418200
---------- MLA ----------
Nogués, G., Kadener, S., Cramer, P., Bentley, D., Kornblihtt, A.R. "Transcriptional activators differ in their abilities to control alternative splicing" . Journal of Biological Chemistry, vol. 277, no. 45, 2002, pp. 43110-43114.
http://dx.doi.org/10.1074/jbc.M208418200
---------- VANCOUVER ----------
Nogués, G., Kadener, S., Cramer, P., Bentley, D., Kornblihtt, A.R. Transcriptional activators differ in their abilities to control alternative splicing. J. Biol. Chem. 2002;277(45):43110-43114.
http://dx.doi.org/10.1074/jbc.M208418200