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ParaplegiaAxonsER SIGNED

Functional interactions between endoplasmic reticulum and mitochondria in Drosophila axons

Total Cost €

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EC-Contrib. €

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Partnership

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 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.

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

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

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 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.

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