Institut for Biomedicin

Søren Lykke-Andersen

Regulatory mechanisms for 3'-end alternative splicing and polyadenylation of the Glial Fibrillary Acidic Protein, GFAP, transcript.

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Regulatory mechanisms for 3'-end alternative splicing and polyadenylation of the Glial Fibrillary Acidic Protein, GFAP, transcript. / Blechingberg, Jenny; Lykke-Andersen, Søren; Jensen, Torben Heick; Jørgensen, Arne Lund; Nielsen, Anders Lade.

I: Nucleic Acids Research, Bind 35, Nr. 22, 2007, s. 7636-50.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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@article{969c48b0cfe411dcabe4000ea68e967b,
title = "Regulatory mechanisms for 3'-end alternative splicing and polyadenylation of the Glial Fibrillary Acidic Protein, GFAP, transcript.",
abstract = "The glial fibrillary acidic protein, GFAP, forms the intermediate cytoskeleton in cells of the glial lineage. Besides the common GFAP alpha transcript, the GFAP epsilon and GFAP kappa transcripts are generated by alternative mRNA 3'-end processing. Here we use a GFAP minigene to characterize molecular mechanisms participating in alternative GFAP expression. Usage of a polyadenylation signal within the alternatively spliced exon 7a is essential to generate the GFAP kappa and GFAP kappa transcripts. The GFAP kappa mRNA is distinct from GFAP epsilon mRNA given that it also includes intron 7a. Polyadenylation at the exon 7a site is stimulated by the upstream splice site. Moreover, exon 7a splice enhancer motifs supported both exon 7a splicing and polyadenylation. SR proteins increased the usage of the exon 7a polyadenylation signal but not the exon 7a splicing, whereas the polypyrimidine tract binding (PTB) protein enhanced both exon 7a polyadenylation and exon 7a splicing. Finally, increasing transcription by the VP16 trans-activator did not affect the frequency of use of the exon 7a polyadenylation signal whereas the exon 7a splicing frequency was decreased. Our data suggest a model with the selection of the exon 7a polyadenylation site being the essential and primary event for regulating GFAP alternative processing. Udgivelsesdato: 2007",
keywords = "Alternative Splicing, Animals, Base Sequence, Cell Line, Cells, Cultured, Exons, Glial Fibrillary Acidic Protein, Humans, Introns, Male, Mice, Molecular Sequence Data, Nuclear Proteins, Polyadenylation, Promoter Regions (Genetics), Protein Isoforms, RNA Splice Sites, RNA Stability, RNA, Messenger, RNA-Binding Proteins, Rats, Transcription, Genetic",
author = "Jenny Blechingberg and S{\o}ren Lykke-Andersen and Jensen, {Torben Heick} and J{\o}rgensen, {Arne Lund} and Nielsen, {Anders Lade}",
year = "2007",
doi = "10.1093/nar/gkm931",
language = "English",
volume = "35",
pages = "7636--50",
journal = "Nucleic Acids Research",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "22",

}

RIS

TY - JOUR

T1 - Regulatory mechanisms for 3'-end alternative splicing and polyadenylation of the Glial Fibrillary Acidic Protein, GFAP, transcript.

AU - Blechingberg, Jenny

AU - Lykke-Andersen, Søren

AU - Jensen, Torben Heick

AU - Jørgensen, Arne Lund

AU - Nielsen, Anders Lade

PY - 2007

Y1 - 2007

N2 - The glial fibrillary acidic protein, GFAP, forms the intermediate cytoskeleton in cells of the glial lineage. Besides the common GFAP alpha transcript, the GFAP epsilon and GFAP kappa transcripts are generated by alternative mRNA 3'-end processing. Here we use a GFAP minigene to characterize molecular mechanisms participating in alternative GFAP expression. Usage of a polyadenylation signal within the alternatively spliced exon 7a is essential to generate the GFAP kappa and GFAP kappa transcripts. The GFAP kappa mRNA is distinct from GFAP epsilon mRNA given that it also includes intron 7a. Polyadenylation at the exon 7a site is stimulated by the upstream splice site. Moreover, exon 7a splice enhancer motifs supported both exon 7a splicing and polyadenylation. SR proteins increased the usage of the exon 7a polyadenylation signal but not the exon 7a splicing, whereas the polypyrimidine tract binding (PTB) protein enhanced both exon 7a polyadenylation and exon 7a splicing. Finally, increasing transcription by the VP16 trans-activator did not affect the frequency of use of the exon 7a polyadenylation signal whereas the exon 7a splicing frequency was decreased. Our data suggest a model with the selection of the exon 7a polyadenylation site being the essential and primary event for regulating GFAP alternative processing. Udgivelsesdato: 2007

AB - The glial fibrillary acidic protein, GFAP, forms the intermediate cytoskeleton in cells of the glial lineage. Besides the common GFAP alpha transcript, the GFAP epsilon and GFAP kappa transcripts are generated by alternative mRNA 3'-end processing. Here we use a GFAP minigene to characterize molecular mechanisms participating in alternative GFAP expression. Usage of a polyadenylation signal within the alternatively spliced exon 7a is essential to generate the GFAP kappa and GFAP kappa transcripts. The GFAP kappa mRNA is distinct from GFAP epsilon mRNA given that it also includes intron 7a. Polyadenylation at the exon 7a site is stimulated by the upstream splice site. Moreover, exon 7a splice enhancer motifs supported both exon 7a splicing and polyadenylation. SR proteins increased the usage of the exon 7a polyadenylation signal but not the exon 7a splicing, whereas the polypyrimidine tract binding (PTB) protein enhanced both exon 7a polyadenylation and exon 7a splicing. Finally, increasing transcription by the VP16 trans-activator did not affect the frequency of use of the exon 7a polyadenylation signal whereas the exon 7a splicing frequency was decreased. Our data suggest a model with the selection of the exon 7a polyadenylation site being the essential and primary event for regulating GFAP alternative processing. Udgivelsesdato: 2007

KW - Alternative Splicing

KW - Animals

KW - Base Sequence

KW - Cell Line

KW - Cells, Cultured

KW - Exons

KW - Glial Fibrillary Acidic Protein

KW - Humans

KW - Introns

KW - Male

KW - Mice

KW - Molecular Sequence Data

KW - Nuclear Proteins

KW - Polyadenylation

KW - Promoter Regions (Genetics)

KW - Protein Isoforms

KW - RNA Splice Sites

KW - RNA Stability

KW - RNA, Messenger

KW - RNA-Binding Proteins

KW - Rats

KW - Transcription, Genetic

U2 - 10.1093/nar/gkm931

DO - 10.1093/nar/gkm931

M3 - Journal article

VL - 35

SP - 7636

EP - 7650

JO - Nucleic Acids Research

JF - Nucleic Acids Research

SN - 0305-1048

IS - 22

ER -