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NeuroUTR

Systematic investigation of the functional coupling between transcriptional and post-transcriptional regulatory interactions underlying tissue-specific 3'UTRs variability.

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

NeuroUTR project word cloud

Explore the words cloud of the NeuroUTR project. It provides you a very rough idea of what is the project "NeuroUTR" about.

protein interactions ing polya network longest engendered characterise integrate aggregation disorders neurodegeneration contributes models untranslated binding sites genomic diseases neurodegenerative site 3 secondary regions types utr specificity mechanisms homeostasis variety tissue transcription platform disrupted regulate ameliorate sequence mutations efficiency regulation therapies extensively underlying incurable bioinformatic stability motor systematically disease translational human associate post rna localisation utrs disorder isoforms systematic proteins mirna variation neurone regulatory mnd cleavage unknown responsible serve transcriptional metabolism linear controls largely cell alternative hypothesise functional structure mrna polyadenylation perturbing genome brain regulating coupling

Project "NeuroUTR" data sheet

The following table provides information about the project.

Coordinator	THE FRANCIS CRICK INSTITUTE LIMITED Organization address address: 1 MIDLAND ROAD city: LONDON postcode: NW1 1AT website: www.crick.ac.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	United Kingdom [UK]
Project website	https://www.crick.ac.uk/research/a-z-researchers/researchers-k-o/nicholas-luscombe/
Total cost	183˙454 €
EC max contribution	183˙454 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2014
Funding Scheme	MSCA-IF-EF-ST
Starting year	2015
Duration (year-month-day)	from 2015-06-01 to 2017-05-31

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	THE FRANCIS CRICK INSTITUTE LIMITED THE FRANCIS CRICK INSTITUTE LIMITED Organization address address: 1 MIDLAND ROAD city: LONDON postcode: NW1 1AT website: www.crick.ac.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	UK (LONDON)	coordinator	183˙454.00
2	CANCER RESEARCH UK LBG CANCER RESEARCH UK LBG Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD website: www.cancerresearchuk.org.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	UK (LONDON)	participant	0.00

Map

Project objective

3' untranslated regions (3' UTRs) serve as a key platform in the RNA regulatory network that controls mRNA translational efficiency, localisation and stability. Of all human cell-types, brain-specific isoforms have the longest 3' UTRs and therefore their regulation is likely to be most complex. Moreover, mutations perturbing the mRNA secondary structure and sites of mRNA-miRNA interactions can lead to diseases such as neurodegeneration. Isoforms of variable 3' UTRs are engendered by alternative cleavage and polyadenylation (polyA) site selection. Of the many factors contributing to this process, both transcriptional and RNA regulatory interactions have been extensively studied. Yet the regulatory mechanisms responsible for the systematic tissue-specific polyA site selection remain largely unknown. Here I hypothesise that changes in transcription factors, RNA binding proteins, and polyA factors activities together regulate the condition-specificity of this process. Furthermore I hypothesise that the resulting 3' UTR sequence variation contributes to increased protein aggregation in neurodegenerative disorders such as motor neurone disease (MND), a common but incurable disorder in which mRNA metabolism and protein homeostasis are disrupted. Here using bioinformatic approaches I will integrate a variety of genomic measurements, and systematically identify tissue-specific transcriptional and post-transcriptional regulatory interactions underlying polyA site selection. I will develop linear models to characterise the genome-wide functional coupling between these regulatory interactions and study how these associate with MND in regulating alternative 3' UTRs. In doing this project I will not only advance our current knowledge about RNA regulation but I will enable a better understanding of the regulatory mechanisms underlying MND, and in the long term, the future development of new therapies that ameliorate the regulation of 3' UTRs in neurodegenerative diseases.

Publications

List of publications.
year	authors and title	journal	last update
2017	Claire E. Hall, Zhi Yao, Minee Choi, Giulia E. Tyzack, Andrea Serio, Raphaelle Luisier, Jasmine Harley, Elisavet Preza, Charlie Arber, Sarah J. Crisp, P. Marc D. Watson, Dimitri M. Kullmann, Andrey Y. Abramov, Selina Wray, Russell Burley, Samantha H.Y. Loh, L. Miguel Martins, Molly M. Stevens, Nicholas M. Luscombe, Christopher R. Sibley, Andras Lakatos, Jernej Ule, Sonia Gandhi, Rickie Patani Progressive Motor Neuron Pathology and the Role of Astrocytes in a Human Stem Cell Model of VCP-Related ALS published pages: 1739-1749, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2017.05.024	Cell Reports 19/9	2019-07-24

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The information about "NEUROUTR" are provided by the European Opendata Portal: CORDIS opendata.