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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.

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

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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