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transLEISHion SIGNED

A targeted knockout screen for identification of Leishmania membrane transporters required for infection of macrophages

Total Cost €

0

EC-Contrib. €

0

Partnership

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 transLEISHion project word cloud

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

amastigote    immune    crispr    proliferates    leishmanias    host    thanks    manipulation    editing    transcriptomic    drug    pathogen    cas9    nutrient    acute    anti    cell    leishmania    roles    urging    phagolysosome    identification    mutants    interactions    sand    48    uncharacterized    parasite    formulations    allowed    promastigote    drugs    throughput    infection    proposes    despite    viability    upregulated    molecular    first    mechanisms    largely    fly    extensively    macrophage    time    defence    modern    efforts    rapid    hitherto    functional    intrinsic    differentiation    agent    encoding    subvert    unexplored    proteins    knockout    surface    generation    systematic    peptidases    drawbacks    hundreds    leishmaniases    mediated    cheaper    world    mexicana    intracellular    transporters    genome    unclear    bite    treatment    attack    genes    biology    cellular    form    gene    survival    causative    harsh    functions    overexpressed    diseases    library    macrophages    kinetoplastida    parasitic    safer    amastigotes    expressed    forms    membrane    disease    transmitted    it   

Project "transLEISHion" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD 

Organization address
address: WELLINGTON SQUARE UNIVERSITY OFFICES
city: OXFORD
postcode: OX1 2JD
website: www.ox.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 195˙454 €
 EC max contribution 195˙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-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-09-01   to  2020-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD UK (OXFORD) coordinator 195˙454.00

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 Project objective

Leishmaniases are among the world's most neglected diseases. It´s causative agent - Leishmania - is transmitted by the bite of a sand fly. In the host, the parasite is taken up by macrophages and proliferates in the harsh conditions of the host phagolysosome. Currently available drugs for treatment present major drawbacks, urging the need for more effective, safer, and cheaper drugs. The molecular and cellular mechanisms that enable Leishmania to subvert macrophage defence mechanisms and cause disease remain largely unclear. Thanks to modern comparative transcriptomic analysis, the identification of hundreds of genes overexpressed in intracellular amastigote forms was possible for the first time and identified cell surface proteins, transporters, peptidases and many uncharacterized genes with possible roles in host-pathogen interactions. Only recently, a high-throughput gene editing method based on CRISPR-Cas9 allowed for the first time easy manipulation of Leishmanias´ complex genome and rapid functional analysis of genes. For over 50 years membrane transporters have been extensively studied in kinetoplastida, due to their role in the intrinsic parasite nutrient needs, defence from host immune attack and uptake of drug formulations. Despite these efforts a large number of such transporters expressed in amastigotes remain uncharacterized. The present project proposes (1) the generation of a library of 48 L. mexicana mutants by systematic CRISPR-Cas9 mediated knockout of amastigote-upregulated genes encoding membrane transporters, (2) Identification of membrane transporters required for viability of the promastigote parasite form and the (3) Identification of membrane transporters required for differentiation into amastigotes, macrophage infection, intracellular survival. The results of this project are expected to provide new insight into functions of hitherto unexplored aspects of amastigote biology and identify potential new targets for anti-parasitic drugs.

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

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