Opendata, web and dolomites

ParaplegiaAxonsER SIGNED

Functional interactions between endoplasmic reticulum and mitochondria in Drosophila axons

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 ParaplegiaAxonsER project word cloud

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

express    experiments    cytosolic    ubiquitously    spastic    interactions    proteins    ubiquity    reep    axon    dysfunction    levels    forms    identification    models    examine    lack    existence    organisation    time    disease    model    regulating    physiological    hereditary    shown    neurons    apparent    continuity    ca2    sensors    laboratory    tubules    architecture    influence    leads    abnormal    er    continuous    paraplegia    cellular    transgenic    concentrations    functions    generate    active    altered    secondly    neuron    colocalisation    axonal    handling    drosophila    genes    mitochondrial    abnormalities    poorly    genotypes    sensor    causative    interplay    sites    resting    arise    mechanisms    host    explore    lumenal    suggested    contact    mitochondria    heterogeneity    nature    protein    first    axons    attempt    degeneration    organelles    degenerative    localised    hsp    modeling    mutants    reticulum    human    roles    network    suitable    function    endoplasmic    encode    appears   

Project "ParaplegiaAxonsER" 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]
 Project website https://www.gen.cam.ac.uk/research-groups/research-groups/okane
 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-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-03-01   to  2019-02-28

 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 183˙454.00

Map

 Project objective

Axonal endoplasmic reticulum (ER) forms a continuous network of tubules that appears to occur ubiquitously in neurons, and has been compared to “a neuron within a neuron”. Its importance is suggested both by its apparent ubiquity, and by the identification of several causative genes for the axon degenerative disease, hereditary spastic paraplegia (HSP), that encode proteins that contribute to ER modeling. However, its physiological roles, and how it could influence axon degeneration, are poorly understood.

There is increasing awareness of the existence, nature and roles of contact sites between ER and other cellular organelles including mitochondria. Here I will explore these interactions and their functions in axons, in particular testing the model that ER architecture is important in regulating mitochondrial function in axons. My host laboratory has recently identified Drosophila mutants that lack one or more relevant HSP genes, and shown abnormalities in the level or continuity of ER in some genotypes.

I will use Drosophila HSP mutants to determine whether mitochondrial abnormalities arise with altered ER organisation. I will also test for colocalisation of a Drosophila Reep protein with ER-mitochondrial contact sites, and whether loss of this protein leads to abnormal mitochondria. Together these experiments will address whether ER-localised HSP proteins affect mitochondrial function.

Secondly I will examine whether mitochondrial Ca2 handling is affected in these models. I will generate transgenic Drosophila that express mitochondrial and cytosolic Ca2 sensors, and attempt to develop a suitable lumenal ER sensor. I will use these to test the levels and heterogeneity of Ca2 concentrations in resting and active axons, and investigate how HSP mutants affect this.

My work will examine the interplay between ER and mitochondria in axons for the first time, and mechanisms of dysfunction that are relevant for human axon degeneration.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "PARAPLEGIAAXONSER" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.3.2.)

MultiSeaSpace (2019)

Developing a unified spatial modelling strategy that accounts for interactions between species at different marine trophic levels, and different types of survey data.

Read More  

LIGHTMATT-EXPLORER (2019)

Experimental determination of the paraxial-vectorial limit of light-matter interactions

Read More  

ActinSensor (2019)

Identification and characterization of a novel damage sensor for cytoskeletal proteins in Drosophila

Read More