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.

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

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.)

Widow Spider Mating (2020)

Immature mating as a novel tactic of an invasive widow spider

Read More  

TARGET SLEEP (2020)

Boosting motor learning through sleep and targeted memory reactivation in ageing and Parkinson’s disease

Read More  

ASIQS (2019)

Antiferromagnetic spintronics investigated by quantum sensing techniques

Read More