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SWI/SNF subunits Brg1 and Brm regulate alternative splicing by interacting with RNA binding proteins in the nascent RNA.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
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(English)Manuscript (preprint) (Other academic)
National Category
Cell and Molecular Biology
Research subject
Cell Biology
Identifiers
URN: urn:nbn:se:su:diva-161375OAI: oai:DiVA.org:su-161375DiVA, id: diva2:1258082
Available from: 2018-10-23 Created: 2018-10-23 Last updated: 2018-10-24Bibliographically approved
In thesis
1. Gene regulation by chromatin remodelling complexes: SWI/SNF complex in mRNA processing and B-WICH complex in ribosomal gene expression
Open this publication in new window or tab >>Gene regulation by chromatin remodelling complexes: SWI/SNF complex in mRNA processing and B-WICH complex in ribosomal gene expression
2018 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The aim of this project is to investigate the roles of chromatin remodelling complexes in gene regulation. It is focused on two groups of chromatin complexes: the mammalian BRG1 and BRM SWI/SNF complexes and the ISWI-containing B-WICH complex.

Study 1 investigates the role of SWI/SNF complexes in alternative splicing. We show that the presence of the ATPase core subunits Brg1 and Brm influence the alternative splicing outcome of a subset of genes. We show that Brg1 and Brm interact with several splicing related factors in the nascent RNA, and that the recruitment of some of these factors to their target sites is regulated by the presence of Brg1 and Brm. We propose that SWI/SNF ATPases can modulate the interactions of RNA binding factors to the nascent RNA and in that way alter alternative splicing outcome.

Study 2 focuses on SWI/SNF complexes and their influence on cleavage and polyadenylation of mRNA. We show that Brg1 and Brm interact with subunits of the cleavage and polyadenylation complexes in the nascent mRNA. SWI/SNF complexes facilitate the recruitment of the cleavage and polyadenylation complex to the polyadenylation site in a subset of genes, and this results in a more efficient cleavage and polyadenylation.

Study 3 shows that B-WICH is required for ribosome gene transcriptional activation upon glucose stimulation. WSTF and SNF2h, two of the B-WICH subunits, are needed to establish an active chromatin state in the RNA pol I gene promoter when the glucose concentration is raised after a period of deprivation. We propose that it counteracts the silent, poised chromatin state imposed by the silencing chromatin remodelling complex NuRD to allow for the RNA pol I machinery to bind to the promoter.

These studies show that the influence of chromatin remodelling complexes upon gene expression is important for remodelling nucleosomes at the promoter, for alternative splicing, cleavage and polyadenylation and transcriptional initiation. These complexes work together with other chromatin remodelling factors, interact with other complexes and regulate their activity by affecting their recruitment dynamics.

Place, publisher, year, edition, pages
Stockholm: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 2018
Keywords
Chromatin remodelling, SWI/SNF, Brg1, Brm, alternative splicing, cleavage and polyadenylation, B-WICH, WSTF, ribosomal genes
National Category
Cell and Molecular Biology
Research subject
Cell Biology
Identifiers
urn:nbn:se:su:diva-161380 (URN)978-91-7797-504-5 (ISBN)978-91-7797-505-2 (ISBN)
Public defence
2018-12-07, Vivi Täckholmsalen (Q-salen), NPQ-huset, Svante Arrhenius väg 20, Stockholm, 09:15 (English)
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Note

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript. Paper 3: Manuscript.

Available from: 2018-11-14 Created: 2018-10-23 Last updated: 2018-11-07Bibliographically approved

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