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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.

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

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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