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Mito-recombine SIGNED

Homologous recombination and its application in manipulating animal mitochondrial DNA

Total Cost €

0

EC-Contrib. €

0

Partnership

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 Mito-recombine project word cloud

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

sequences    isolate    manipulating    incurable    regarding    screen    largely    genetic    mapping    phenotypic    genetically    mitochondrial    copy    accelerate    health    mutations    possibilities    heteroplasmic    genome4    energy    site    progeny    map    differences    fly    recombination    variations    select    mutagenesis    sites    rnai    undergo    influences    dna    functions    induce    evolution    disease    first    organismal    colleague    genome    homologous    traits    metabolic    works    diseases    powerful    possibility    establishing    existence    allowed    demonstrated    biology    functional    directed    impacts    inability    recombinant    candidate    drosophila    animal    diseases1    snps    time    limited    mtdna    components    transform    cellular    introduce    nuclear    ways    machinery    mitochondria    trait    mutants    tools    opens    containing    organisms    manipulate    inherited    toolkit    link    involvement    create    disorders    genotypes2    date    showed   

Project "Mito-recombine" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.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]
 Total cost 1˙473˙732 €
 EC max contribution 1˙473˙732 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-STG
 Funding Scheme ERC-STG
 Starting year 2019
 Duration (year-month-day) from 2019-03-01   to  2024-02-29

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 1˙473˙732.00

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 Project objective

Mitochondrial DNA (mtDNA) is a multi-copy genome that works with the nuclear genome to control energy production and various cellular processes. To date, disorders associated with mutations in mtDNA are among the most common genetically inherited metabolic diseases1. However, our knowledge regarding many aspects of mtDNA biology remains limited, and we know even less about how it influences development and organismal traits. This is largely due to our inability to manipulate mtDNA. Recently, a colleague and I developed novel genetic tools in Drosophila that allowed us to isolate animal mitochondrial mutants for the first time, and to create heteroplasmic organisms containing two mitochondrial genotypes2,3. These advances make Drosophila a powerful system for mtDNA studies. Importantly, I showed that Drosophila mtDNA could undergo homologous recombination. Furthermore, I established a system to induce recombination at specific sites and select for progeny containing only the recombinant genome4. Thus, my work has demonstrated the existence of recombination in animal mitochondria, and opens up the possibility of developing a recombination system for functional mapping and manipulating animal mtDNA. Here I propose to 1) identify components of the mitochondrial recombination machinery by a candidate RNAi screen; 2) develop a recombination toolkit to map trait-associated mtDNA sequences/SNPs; and 3) build a site-directed mutagenesis system by establishing robust ways to deliver DNA into fly mitochondria. Given the essential functions of mitochondria and their involvement in incurable diseases, the genetic tools developed in this proposal will transform the field by making it possible to link mtDNA variations to phenotypic differences and introduce specific mutations into mtDNA for functional studies at organismal level. These advances will open many possibilities to accelerate our understanding on how mtDNA impacts health, disease and evolution.

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