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Sulphirulence

Re-engineering of fungal sulphur metabolism to limit mould viability and virulence.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 Sulphirulence project word cloud

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

regulation    essentiality    discovered    mould    clinical    sole    eukaryotic    homocysteine    synthesis    designing    vivo    molecule    pathogen    h2s    deficient    human    expertise    oxidized    illnesses    mutants    world    secondary    therapies    eliminated    cells    fungus    sources    experimental    mice    enforce    annum    viability    host    appears    seek    view    million    aspergillus    fumigatus    biosynthesis    precursor    decipher    fungal    harness    wish    disease    gt    genome    transgenic    synthase    foremost    respectively    intact    inorganic    requirement    enzyme    proteins    transcriptome    virulence    source    exploitable    blockade    candidate    precise    cysteine    assimilation    scientific    occurrence    pathogenicity    antifungal    sequences    methionine    sulfhydration    leaving    correlates    exploited    responsible    gaseous    function    infection    mammalian    mutational    sulphur    class    containing    molecular    signalling    snps    lungs    scrutinizing   

Project "Sulphirulence" data sheet

The following table provides information about the project.

Coordinator
THE UNIVERSITY OF MANCHESTER 

Organization address
address: OXFORD ROAD
city: MANCHESTER
postcode: M13 9PL
website: www.manchester.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 183˙454 €
 EC max contribution 183˙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-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-02-01   to  2018-01-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF MANCHESTER UK (MANCHESTER) coordinator 183˙454.00

Map

 Project objective

Aspergillus fumigatus, the major mould pathogen of human lungs, is responsible for > 2 million illnesses per annum in Europe . I have discovered that sulphur is an essential host-derived element during A. fumigatus infection . This finding is novel, and highly exploitable as a) Synthesis of the sulphur-containing molecule methionine appears to be essential for viability of A. fumigatus b) Regulation of sulphur assimilation is essential for A. fumigatus virulence and c) The foremost candidate sulphur source in mammalian lungs (H2S) is gaseous, and recently identified as a novel signalling molecule in eukaryotic cells . I now wish to harness world-class clinical and scientific expertise in the field of fungal pathogenicity to identify the precise molecular source of sulphur exploited by A. fumigatus during experimental and clinical infection, with a view to designing novel antifungal therapies. OBJECTIVES 1. To define the role of methionine synthase in A. fumigatus viability I will enforce a mutational blockade upon biosynthesis of the sole methionine precursor, homocysteine, while leaving methionine synthase intact. This will decipher between essentiality of methionine biosynthesis, and essentiality of a secondary function of the methionine synthase enzyme. 2. I have eliminated cysteine and oxidized inorganic-S sources as in-host sources of sulphur. I will now address, via mutational analysis in the fungus, in-host transcriptome and transgenic mice whether methionine or H2S are exploited in the host. Having defined the S-source exploited in vivo, I will seek correlates with human disease by scrutinizing human and fungal genome sequences for SNPs associated, respectively, with human H2S production and fungal sulphur assimilation. 3. I will use A. fumigatus mutants deficient in production and assimilation of H2S to address the occurrence of, and requirement for, sulfhydration of fungal proteins during mammalian infection.

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