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transLEISHion SIGNED

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

Total Cost €

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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.

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

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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