-------- Original Message -------- Subject: FW: Systems Biology for PNS disease? Date: Fri, 4 Jul 2008 16:07:03 +0200 From: Timmerman Vincent <vincent.timmerman@ua.ac.be> To: <yves.vandepeer@psb.ugent.be> __________________________________________ *From:* Timmerman Vincent *Sent:* Friday, July 04, 2008 4:03 PM *To:* Yves Van de Peer (_yvdp@gengenp.rug.ac.be) _*_Cc_* <mailto:yvdp@gengenp.rug.ac.be%29Cc>*:* Leonardo de Almeida Souza ; sophie janssens *Subject:* Systems Biology for PNS disease? Dear Yves, As I enjoyed your presentation on “Systems Biology” at the VIB DC meeting in June, I would like to come back at our discussion we had. As you know we are studying the molecular genetics and cell biology of the peripheral nervous system (PNS). In particular we study the inherited forms of PNS disease, resulting in peripheral nerve degeneration. Up to date we have 40 genes and more than 800 mutations in these genes causing various types of peripheral neuropathies. For many of these genes, their protein function is “unknown” or it remains a mystery why mutations in these proteins are associated with neurodegeneration. As an example we identified mutations in small heat shock protein genes (HSPB1 and HSPB8) causing motor neuropathies, mutations in amino-acyl-tRNA synthetases (YARS, GARS) causing variants of Charcot-Marie-Tooth (CMT) neuropathies, mutations in small GTP-ases and GEF proteins causing other variants of CMT, etc. Other genes make sense since these are implicated in Schwann-cell biology and myelination, or axonal transport. You can find on this link (_http://www.molgen.ua.ac.be/CMTMutations/_) a database that we developed over the years showing the genes involved and the mutations identified so far in peripheral neuropathies. It would be very interesting and timely to run one of your bio-informatic platforms to compare the wild type protein-protein interaction networks between these 40 known genes, with the mutant protein-protein interactions. This is of interest since we are currently hunting for differential interacting molecular partners (wild type versus mutant) for some of the genes we are currently focusing on in one of our research projects (through TAP purification and mass-spectrometry). The identification of small (or major: although unlikely) differences between wild type and patient/mutation specific protein interaction networks would provide novel insights into which “novel” proteins or genes could explain the neuronal specificity. Would it be possible to meet with you and your colleagues this summer or in September to see what is feasible at the bio-informatics level with the hope to detect some interacting genes that could be relevant for neuropathies. FYI: I will be on holiday in August (1-23). With my best and friendly greetings, Vincent Prof. Dr. Vincent Timmerman, PhD VIB - Department of Molecular Genetics Peripheral Neuropathy Group University of Antwerp - CDE Parking P4, Building V, Room 1.30 Universiteitsplein 1 BE-2610 Antwerpen Belgium Tel: +32-3-265.10.24 Tel: +32-3-265.10.02 (Secretary VIB8: Mrs. Gisèle Smeyers) Fax: +32-3-265.10.12 E-mail: _vincent.timmerman@ua.ac.be_ <mailto:vincent.timmerman@ua.ac.be> _http://www.molgen.ua.ac.be/_ _http://www.molgen.ua.ac.be/CMTMutations/_ -- Yves Van de Peer, PhD. Professor in Bioinformatics and Genome Biology Group Leader Bioinformatics and Evolutionary Genomics VIB Department of Plant Systems Biology, UGent Ghent University Technologiepark 927 B-9052 Ghent Belgium Phone: +32 (0)9 331 3807 Cell Phone: +32 (0)476 560 091 Fax: +32 (0)9 331 3809 email: yves.vandepeer@psb.ugent.be http://bioinformatics.psb.ugent.be/