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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.

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

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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