PARAPLEGIA ENDOSOMES

Spastic paraplegia genes and endosomal signaling in Drosophila

Coordinatore	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE    more  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Edna Cognome: Murphy Email: send email Telefono: +44 1223 333543 Fax: +44 1223 332988
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	0 €
EC contributo	170˙733 €
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-IEF-2008
Funding Scheme	MC-IEF
Anno di inizio	2009
Periodo (anno-mese-giorno)	2009-10-12   -   2011-10-11

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Edna Cognome: Murphy Email: send email Telefono: +44 1223 333543 Fax: +44 1223 332988	UK (CAMBRIDGE)	coordinator	170˙733.61

Mappa

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 Obiettivo del progetto (Objective)

'The hereditary spastic paraplegias (HSPs) are a group of neurodegenerative conditions characterised by the degeneration of longer spinal cord motor tract axons. The normal function of the 13 cloned spastic paraplegia genes (SPGs) is largely unknown, but most encode intracellular membrane-associated proteins. Recently, the host laboratory has established that one of these genes, SPG6, encodes an endosomal regulator of BMP receptor trafficking, and regulates synaptic growth and axonal microtubules via this effect. The aim of this project is to test whether other intracellular membrane SPG products also function in receptor membrane trafficking and signalling, particularly in the BMP pathway. The focus of the study will be on the three SPGs currently most amenable to study in Drosophila melanogaster, a model system with proven power in this area. Top priority will be given to the recently identified spastizin (SPG15), an endosomal localised protein containing a FYVE motif, found on proteins that function in the regulation of endocytic trafficking. Mutants of the Drosophila SPG15 homologue will be generated to study phenotypes, particularly at the neuromuscular junction (NMJ). Also, antibodies will be generated to investigate spastizin colocalisation and association with BMP, Wnt, and Notch pathway subunits. In addition, I will use similar approaches to test two other membrane associated SPG products: spastin (SPG4) and atlastin (SPG3A). These are among the most commonly mutated SPGs, thus Drosophila stocks and reagents are already available, but their potential role in regulating endosomal trafficking pathways is not well studied. This investigation, into the functional pathways of spastizin, spastin, and atlastin, will further the understanding of the mechanism of action of mutated proteins in motor neuron degeneration.'