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Mechanisms of Myelination – Elucidating the Diversity of Oligodendroglial Precursors and their Local Axon-Glia Interactions

Total Cost €


EC-Contrib. €






 MecMy project word cloud

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

myelinated    organism    form    communication    time    local    precursor    organ    dynamics    nervous    regulatory    oligodendroglial    interactions    fails    specification    cells    tract    principles    differentiation    functional    fundamentally    axon    signal    mechanistic    cell    reveal    device    subcellular    structure    causal    axons    glia    suited    first    memory    molecular    learning    transmission    precursors    animal    imaging    manipulation    population    lifelong    specialized    global    oligodendroglia    intrinsic    signature    interaction    heterogeneity    inefficient    damage    neurons    extrinsic    elucidate    repair    myelination    precise    myelin    genetic    mediators    clonal    strategies    individual    lastly    glial    unclear    survival    underlying    model    normal    disease    live    vivo    employ    abundant    function    myriads    ensures    ideally    diverse    insights    goals    surrounded    insulating    diversity    generate    cellular    zebrafish    mechanisms    regulating    carry    fast   

Project "MecMy" data sheet

The following table provides information about the project.


Organization address
address: Arcisstrasse 21
postcode: 80333

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 Germany [DE]
 Total cost 1˙485˙000 €
 EC max contribution 1˙485˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2016-STG
 Funding Scheme ERC-STG
 Starting year 2017
 Duration (year-month-day) from 2017-02-01   to  2022-01-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

Nervous system function requires precise communication between myriads of neurons and glia to generate and maintain a functional organ. Most axons are eventually surrounded with myelin, an insulating structure produced by specialized oligodendroglia. This cellular interaction enables fast signal transmission, ensures long-term axon survival, and is involved in regulating learning and memory formation. The formation of new myelin during lifelong development and after myelin damage requires differentiation of oligodendroglial precursors. Although these cells are an abundant population, myelin repair is often inefficient and eventually fails. It is known that oligodendroglial precursors have diverse properties, but whether this diversity is at any level a regulatory factor for normal myelination, or causal to failure of myelin repair is unclear. Here, I will elucidate the diversity of oligodendroglial precursors by carrying out the first global analysis of their population dynamics in the whole animal from specification to myelination. I will investigate how differentiation properties change over time, reveal whether this is due to intrinsic or extrinsic factors, and identify the underlying molecular mechanisms. To achieve these goals I will use zebrafish, an ideally suited model organism for in vivo live cell imaging and genetic manipulation. I will carry out a clonal analysis of oligodendroglial precursor population dynamics during myelinated tract formation and after myelin damage. I will analyse the molecular signature of cells with different properties to identify crucial mediators. Lastly, I will investigate whether individual cells can show diversity at the subcellular mechanistic level of local axon-glial interactions. My work will provide fundamentally new insights into the principles of the heterogeneity of oligodendroglial precursors and may help to device new strategies of how to employ these cells to form new myelin in development and disease.

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