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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.

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

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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