Control of alternative pre-mRNA splicing by RNA pol II elongation: Faster is not always better
The realization that the mammalian proteomic complexity is achieved with a limited number of genes demands a better understanding of alternative splicing regulation. Promoter control of alternative splicing was originally described by our group in studies performed on the fibronectin gene. Recently,...
| Autores: | , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2003 |
| País: | Argentina |
| Institución: | Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
| Repositorio: | Biblioteca Digital (UBA-FCEN) |
| Idioma: | inglés |
| OAI Identifier: | paperaa:paper_15216543_v55_n4-5_p235_Nogues |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_15216543_v55_n4-5_p235_Nogues |
| Access Level: | acceso abierto |
| Palabra clave: | Alternative splicing Elongation mRNA processing RNA polymerase II Transcription calcitonin gene related peptide fibronectin Hermes antigen messenger RNA protein proteome transcription factor alternative RNA splicing animal cell controlled study cystic fibrosis DNA template gene control gene function genetic code genetic transcription mammalian genetics nonhuman promoter region protein RNA binding proteomics regulatory mechanism review Alternative Splicing Animals Models, Genetic RNA Polymerase II RNA Precursors RNA, Messenger RNA-Binding Proteins Transcription, Genetic Animalia Mammalia |
| Sumario: | The realization that the mammalian proteomic complexity is achieved with a limited number of genes demands a better understanding of alternative splicing regulation. Promoter control of alternative splicing was originally described by our group in studies performed on the fibronectin gene. Recently, other labs extended our findings to the cystic fibrosis, CD44 and CGRP genes strongly supporting a coupling between transcription and pre-mRNA splicing. A possible mechanism that would fit in these results is that the promoter itself is responsible for recruiting splicing factors, such as SR proteins, to the site of transcription, possibly through transcription factors that bind the promoter or the transcriptional enhancers. An alternative model, discussed more extensively in this review, involves modulation of RNA pol II (pol II) elongation rate. The model is supported by findings that cis- and trans-acting factors that modulate pol II elongation on a particular template also provoke changes in the alternative splicing balance of the encoded mRNAs. |
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