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TransSplicHD

Single-Cell Transcriptomics and Spliceosome analysis to uncover new mechanisms of neuronal vulnerability to Huntington’s Disease.

Total Cost €

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EC-Contrib. €

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Partnership

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 TransSplicHD project word cloud

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

woman    competitive    knock    expression    putamen    consolidate    prevailing    msca    manner    vulnerability    aberrant    htt    medium    connections    scientific    msn    leads    truly    exposure    transcriptional    striatum    hd    hypothesis    cag    drd2    cellular    transition    striatal    cerebellar    single    biological    ultimately    cortical    training    human    independent    cibio    postdoctoral    mouse    synthesis    genome    cell    host    hdh    expertize    disease    dominant    behavioral    neurons    initial    regulation    context    academic    gene    ri    area    spiny    allele    alterations    perfectly    rna    mainly    skills    caudate    laser    implications    disentangle    huntingtin    expansion    transcription    global    drd1    ki    neuroanatomical    integration    direct    deeper    am    capture    optimally    neuronal    mutation    neurodegenerative    deregulation    benefit    supervisor    exchange    mutant    indirect    investigator    career    repeat    positioned    caused    biogenesis    alternative    copy    death    huntington    instrumental    pathological    blend    splicing    molecular    genetic    believe    dissection    neuroscience    rnaseq    disorders    pis    expertise    neurobiology    accurate    events    models   

Project "TransSplicHD" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI TRENTO 

Organization address
address: VIA CALEPINA 14
city: TRENTO
postcode: 38122
website: www.unitn.it

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 Italy [IT]
 Project website https://www.cibio.unitn.it/184/neuroepigenetics-laboratory AND https
 Total cost 180˙277 €
 EC max contribution 180˙277 € (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-RI
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2018-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI TRENTO IT (TRENTO) coordinator 180˙277.00

Map

 Project objective

Huntington’s disease (HD) is neurodegenerative disease caused by a CAG repeat expansion mutation in the HTT gene. The pathological process, which ultimately leads to neuronal loss mainly in the caudate and putamen, is induced - in a truly dominant manner - by a single copy of the mutant allele. Transcriptional deregulation has becoming a prevailing feature in HD and changes at single-gene level in RNA biogenesis and aberrant alternative splicing (AS) events have been associated to neuronal vulnerability. Here, I propose to disentangle at genome-wide level the connections between mutant huntingtin expression and RNA processing, and its implications for neuronal vulnerability to death. Specifically, I propose to study alterations in RNA transcription and AS in: Aim 1. Striatal, cortical and cerebellar areas of Hdh knock-in (KI) HD accurate mouse models through global RNAseq; Aim 2. In specific medium spiny neurons (MSN) of the Drd1 or Drd2 direct and indirect pathways of Hdh KI striatum through laser capture dissection and single-cell RNAseq. The present research proposal represents a synthesis of my interest, expertise in RNA regulation, genome-wide approaches and single-cell analysis in the context of neurodegenerative disorders with my most recent exposure to human genetic. On the other hand, at the CIBIO host institution I will greatly benefit from the scientific exchange with the PIs of the neurobiology area, and my supervisor in particular, whose skills in neuroscience, neuroanatomical and behavioral analyses will perfectly blend and consolidate my cellular and molecular expertize. Thus, I believe I am optimally positioned to accomplish the aims of the current application: the MSCA-RI-IF will be instrumental to develop this initial hypothesis into deeper biological understanding of HD and represent a crucial support to my scientific integration as a competitive, woman investigator in the transition from postdoctoral training to an independent academic career.

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

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