Abstracts
- 09/01/2012 - V. A. Huynh-Thu
- 09/01/2012 - R. Küffner
- 09/01/2012 - C. Ambroise
- 16/09/2011 - M. Bunster
- 27/04/2011 - P. Meyer
- 06/04/2011 - D. Débois
- 30/03/2011 - J. Wouters
- 28/01/2011 - J.-C. Lambert
- 13/12/2010 - J. Giard
- 17/11/2010 - B. Charloteaux
- 12/05/2010 - P. Soumillion
- 30/04/2010 - J.-P. Vert
- 14/04/2010 - X. Tordoir
- 24/03/2010 - J.C. Voegel
- 17/03/2010 - A. Turtoi
- 24/02/2010 - L. Palmeira
- 27/01/2010 - D. Devos
- 09/12/2009 - F. Heuze
- 25/11/2009 - L. Geris
- 19/11/2009 - V. Gabelica
- 14/10/2009 - G. Zocchi
- 30/09/2009 - K. Van Steen
- 12/06/2009 - D. Gianola
- 05/06/2009 - F. J. Theis
- 02/06/2009 - M. Babu
- 07/05/2009 - J. Eyzaguirre
- 22/04/2009 - E. Bullinger
- 08/04/2009 - F. Francis
- 04/03/2009 - Kick-off
Phenotypic outcomes of edgetic perturbations
Benoit Charloteaux
Date and place: Wednesday November, 17th 12:30 pm at Amphi Stainier (B36)
Phenotypic variations of an organism may arise from alterations of cellular networks, ranging from the complete loss (or addition) of a gene product to the specific perturbation of a single molecular interaction. In interactome networks modeled as nodes (macromolecules) connected by edges (interactions), these alterations can be thought of as node removal (or addition) and edge-specific or “edgetic” perturbations, respectively. We show that taking into account interactome network alterations should help to better understand complex genotype-to-phenotype relationships. In particular, we demonstrate that edgetic perturbations can affect biological systems as significantly as node removals. Modeling network perturbations induced by mutations associated with human Mendelian disorders, we show that the nature of the network perturbation (node removal versus edgetic perturbations) partly account for the complexity of genotype-to-phenotype relationships[1]. We then investigate the extent to which edgetic modifications might be the basis of evolution by gene duplication. Lastly, using the C. elegans antiapoptotic protein CED-9, we demonstrate that the systematic isolation of edgetic alleles and their characterization in vivo represents a promising strategy to investigate gene function(s)[2].
[1]. Zhong, Q., Simonis, N., Li, Q. R., Charloteaux, B., Heuze, F., Klitgord, N., et al. (2009) Edgetic perturbation models of human inherited disorders. Mol Syst Biol 5, 321.
[2]. Dreze, M., Charloteaux, B., Milstein, S., Vidalain, P. O., Yildirim, M. A., Zhong, Q., et al. (2009) 'Edgetic' perturbation of a C. elegans BCL2 ortholog. Nat Methods 6, 843-9.