CNVIMPACTGEXP

Deep surveying of CNV impact on Mouse transcriptome complexity and regulation

Coordinatore	more  Organization address city: LAUSANNE postcode: 1015 contact info Titolo: Prof. Nome: Alexandre Cognome: Reymond Email: send email Telefono: +41 21 692 3961 Fax: +41 21 692 3965
Nazionalità Coordinatore	Non specificata
Totale costo	180˙470 €
EC contributo	180˙470 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-06-01   -   2012-10-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE DE LAUSANNE  Organization address city: LAUSANNE postcode: 1015 contact info Titolo: Prof. Nome: Alexandre Cognome: Reymond Email: send email Telefono: +41 21 692 3961 Fax: +41 21 692 3965	CH (LAUSANNE)	coordinator	180˙470.80

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 Obiettivo del progetto (Objective)

'Copy number variation (CNV) of DNA segments has recently been identified as a major source of genetic diversity, but a comprehensive understanding of the phenotypic effect of these structural variations is only beginning to emerge. An extensive map of CNV in wild mice and inbred strains has been established by the host group. These variable regions cover ~11% of their autosomal genome. CNVs are suggested to shape tissue transcriptomes on a global scale and thus represent a substantial source for within-species phenotypic variation. In this context, we address three major research objectives all regarding the impact of structural variants on different aspects of the transcriptome. To unravel the effects of CNVs on expression at the nucleotide rather than locus level we propose to use RNA-seq to monitor expression changes of both coding and non-coding RNAs that map to or close to genomic regions that vary in copy numbers in multiple tissues of the three mouse inbred strains (129S2, DBA/2J, C57BL/6J). These will be compared to changes in the abundance of transcripts that lie outside of CNV regions. Secondly, we will use RNA-seq data to identify and characterize alternative splicing events that are either tissue- or strain-specific, as well as determine whether copy number polymorphisms affect this process. Thirdly, we will investigate allelic imbalance at genome-wide scale and check if this phenomenon is more likely to occur in CNVs. This work should (i) give an unprecedented global and precise view of the mouse transcriptome; (ii) produce the first transcriptome comparison at the nucleotide level of normal individuals of a population; (iii) help to gauge the influence of CNVs on the transcriptome and (iv) provide the first assessment of allelic imbalance at genome-wide scale.'