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.

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

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.)

MingleIFT (2020)

Multi-color and single-molecule fluorescence imaging of intraflagellar transport in the phasmid chemosensory cilia of C. Elegans

Read More  

DEMOS (2019)

Disfluencies and Eye MOvements during Speech: what can they reveal about language production?

Read More  

MathematicsAnalogies (2019)

Mathematics Analogies

Read More