NRVINTEGRATIONMODEL

A model system to study host genome dynamics mediated by integration of non-retroviral RNA virus

 Coordinatore THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE 

 Organization address address: The Old Schools, Trinity Lane
city: CAMBRIDGE
postcode: CB2 1TN

contact info
Titolo: Ms.
Nome: Renata
Cognome: Schaeffer
Email: send email
Telefono: +44 1223 333543
Fax: +44 1223 332988

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 211˙092 €
 EC contributo 211˙092 €
 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-PEOPLE-2010-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-09-19   -   2013-09-18

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE

 Organization address address: The Old Schools, Trinity Lane
city: CAMBRIDGE
postcode: CB2 1TN

contact info
Titolo: Ms.
Nome: Renata
Cognome: Schaeffer
Email: send email
Telefono: +44 1223 333543
Fax: +44 1223 332988

UK (CAMBRIDGE) coordinator 211˙092.80

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

demonstrated    host    lcmv    induced    cells    rna    model    mechanisms    virus    sequences    retroviral    dynamics    integration    reported    nrv    carry    nrvs    segment    dna    respective    genome    viruses    implications   

 Obiettivo del progetto (Objective)

'Genome dynamics is known to be affected by abiotic and biotic factors which enrich the diversity among cells and individuals of the same species. Stress induced by pathogens has been demonstrated to impact host genome stability, but little is known about the effect of non-retroviral RNA viruses (NRVs). NRVs carry a RNA genome and no DNA stage is involved during its infection cycle. Therefore, integration of NRVs' sequences into its host genome is not expected. Despite that, integration of a NRV segment into the host genome has been reported in mammals, plants, insects, fungi and bacteria and was suggested to raise new host phenotypes. Additionally, integration of a host segment within a defective NRV's genome has also been reported demonstrating reciprocal sequence exchange between NRV and its host. Although it has been demonstrated that NRV retrotransposition occurs, the nature of that NRV-mediated host divergence is not clear. Here we propose to further investigate the mechanisms and implications of host-genome plasticity due to NRV integration by building a molecular NRV integration model based on the Lymphocytic Choriomeningitis Virus (LCMV), which has been found integrated within its respective hosts genome, the mouse (Mus musculus) as well as the human. This LCMV-based system is design to carry an integration-induced selective marker, which is assumed to enable identification of cells carrying a DNA version of LCMV-derived sequences in vitro and in vivo. Through combining this experimental system with data analysis, it is likely that we'll be able to initiate, select and track such LCMV-derived integration events. The aforementioned system will serve as a model to determine LCMV's integration frequency, mechanisms, as well as possible implications such as somatic and heritable genetic disorders and virus resistance/tolerance phenotype, triggered by non-retroviral RNA viruses' dynamics with their respective host genomes.'

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