CCMEBAZ

Molecular basis of cell communication during a migratory event that establishes brain asymmetry in zebrafish

 Coordinatore UNIVERSITY COLLEGE LONDON 

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Greta
Cognome: Borg-Carbott
Email: send email
Telefono: +44 (0) 2031083033
Fax: +44 (0)20 78132849

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 181˙103 €
 EC contributo 181˙103 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2009-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-03-01   -   2013-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Greta
Cognome: Borg-Carbott
Email: send email
Telefono: +44 (0) 2031083033
Fax: +44 (0)20 78132849

UK (LONDON) coordinator 181˙103.20

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 Word cloud

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neighbouring    primordium    brain    mechanisms    signalling    activation    molecular    migration    asymmetry    determine    pathway    autonomously    parapineal    cells    establishing    reporter    fgf   

 Obiettivo del progetto (Objective)

'The long-term aim of the proposed study is to resolve the genetic and cell biological mechanisms that contribute to the establishment of vertebrate brain asymmetry. In the zebrafish forebrain, an event crucial in establishing and elaborating asymmetry is the migration of the parapineal primordium. Parapineal cells are specified bilaterally at the midline. They subsequently assemble into a rosette-like structure and migrate to the left side of the brain. The molecular basis of the cellular communication among the parapineal cells during migration is still poorly understood. Preliminary data in Dr Wilson’s group show that Fgf8 induces highly focal pathway activation prior to and during migration. Fgf-reporter activation is found only in one or a few cells that are likely at the leading edge of the migrating primordium. This reporter activation occurs concurrently with suppression of activity in adjacent cells. Our hypothesis is that Fgf pathway activation non-autonomously suppresses pathway activity in neighbouring cells thereby establishing polarity within the entire primordium. In the proposed project, I will utilise multiple techniques to address specific questions with the following immediate aims: 1) to establish how localised activation of Fgf signalling correlates with parapineal migration; 2) to determine how Fgf pathway activation non-autonomously regulates pathway activity in neighbouring cells by addressing the roles of candidate interacting pathways (Notch and Wnt); 3) to determine the molecular mechanisms that govern the cross-talk between Fgf signalling and any of the identified candidates in aim 2.'

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