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Myel-IN-Crisis SIGNED

Myelin at the crossroads of Development and Disease

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EC-Contrib. €

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Partnership

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 Myel-IN-Crisis project word cloud

Explore the words cloud of the Myel-IN-Crisis project. It provides you a very rough idea of what is the project "Myel-IN-Crisis" about.

sclerosis    nerve    underlie    smart    extrinsic    proteolipid    initiation    developmental    undergo    preliminary    precisely    stroke    intensively    function    termination    myelin    fold    hypoxia    merzbacher    death    biology    defects    usr    mammalian    extraordinary    questions    area    leads    protein    accomplished    apoptotic    sensor    mtor    transient    oligodendrocyte    lipid    generate    disease    nervous    machinery    dramatic    cerebral    translational    preterm    isp    roles    translation    synthetic    transcriptional    infants    overloaded    cns    myelinating    transcription    energy    palsy    substance    dysregulation    central    single    iron    pmd    extensions    axons    risk    day    metamorphosis    nutrient    oxygen    stress    surface    strategies    crisis    diseases    multiple    matter    feat    hif    plp1    universal    differentiation    coordinates    upregulated    intrinsic    pelizaeus    fatal    lack    injury    put    myel    mechanisms    oligodendrocytes    mutant    leukodystrophy    rescue    either    6500    human    white    synthesis    toxic    indicate    mutation    myelination    metabolic    controls    cell    regulating   

Project "Myel-IN-Crisis" 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 2˙500˙000 €
 EC max contribution 2˙500˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-ADG
 Funding Scheme ERC-ADG
 Starting year 2018
 Duration (year-month-day) from 2018-10-01   to  2023-09-30

 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 2˙500˙000.00

Map

 Project objective

The oligodendrocyte, the largest cell in mammalian biology, greatly enables central nervous system (CNS) function through production of a single substance: myelin. Oligodendrocytes undergo a dramatic 1-2 day metamorphosis during myelination, increasing their cell surface area ~6500-fold with proteolipid extensions to nerve axons in the CNS white matter. How is this synthetic feat accomplished? We lack a comprehensive understanding of machinery that precisely coordinates transcription, translation, lipid synthesis and energy production. Moreover, how do these mechanisms become so intensively upregulated during myelination? Does this extraordinary transient state put the myelinating oligodendrocyte at risk of death in diseases of white matter? These questions underlie the Aims of the proposal “Myel-IN-crisis.” I propose (Aim 1) testing whether an “Integrated Synthetic Programme (ISP)” controls oligodendrocyte differentiation, metabolic and synthetic requirements of developmental myelination. In Aim 2, I will investigate roles for “smart sensor” oxygen (HIF) and nutrient (mTOR) pathways in regulating initiation and termination of the ISP. During development, extrinsic white matter injury in preterm infants leads to cerebral palsy, while intrinsic defects in myelin protein PLP1 cause the fatal human leukodystrophy, Pelizaeus-Merzbacher disease (PMD). Preliminary studies indicate transcriptional and translational dysregulation in human PLP1-mutant oligodendrocytes, which become iron overloaded leading to apoptotic cell death. In Aim 3, I propose that either extrinsic (e.g., hypoxia) or intrinsic (e.g., PLP1 mutation) factors promote a “Universal Stress Response (USR)” in the pre-myelinating oligodendrocyte that leads to toxic dysregulation of the ISP. Finally, in Aim 4 we will identify the key pathways of the USR to generate strategies for rescue of myelination with potential translational impact in cerebral palsy and leukodystrophy, multiple sclerosis and stroke.

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