Lejeune et al. BMC Genomics 2012, 13:91 http://www.biomedcentral.com/1471-2164/13/91 Additional file 5: Table S4. List of the 15 genes that modified 19Q- neuron dysfunction when knocked-down by RNAi. Additional file 6: Table S5. List of the 15 genes that modified 128Q- neuron dysfunction in the secondary screen and were previously reported to modify polyQ aggregation when knocked-down by RNAi. Additional file 7: Table S6. Gene Ontology classification of genes that suppressed 128Q-neuron dysfunction when knocked-down by RNAi. Additional file 8: Table S7. Gene Ontology classification of genes that aggravated 128Q-neuron dysfunction when knocked-down by RNAi. Additional file 9: Table S8. Modules (n = 137) generated by network- boosted analysis for suppression of 128Q-neuron dysfunction by RNAi. Additional file 10: Table S9. Modules (n = 105) generated by network- boosted analysis for aggravation of 128Q-neuron dysfunction by RNAi. Acknowledgements We are grateful to Cheryl Wellington and Michael Hayden (University of British Columbia, Canada) for providing constructs encoding htt with 128 Glns and Jean Philippe Vert for help with bioinformatics. We thank Hazare Nouari, David Bragado, Salima Abderrahmane, Sabine Cleofax, and Sidonie Vivequin for technical assistance, and Jim Wang and George Yohrling (CHDI Foundation) for lists of genes involved in autophagy, mitochondrial activity, and synaptic activity. J.A.P. was supported by a Young Researcher Award from Inserm. R.V. is supported by a Poste Vert fellowship from Inserm. This work was supported by Inserm, the Agence Nationale de la Recherche (ANR), the Fondation pour la Recherche Médicale (FRM), Paris, France, the Hereditary Disease Foundation (USA) and the European Huntington Disease Network (Euro-HD, Germany). Author details 1INSERM, Unit 894, Laboratory of Neuronal Cell Biology and Pathology, 75014 Paris, France. 2University of Paris Descartes, EA 4059, 75014 Paris, France. 3Université de Montreal, CRCHUM Centre d’excellence en neuromique, Hôpital Notre-Dame, Montreal, QC,H2W 1T8 Canada. 4Mines ParisTech, CBIO, Fontainebleau, 75006 Paris, France. 5Curie Institute, Research Center, 75005 Paris, France. 6INSERM, Unit 900, Paris, 75005 France. 7Buck Institute, Novato, CA 94945, USA. Authors’ contributions FXL, LM and FP designed and performed data analysis and developed database tools. CB contributed to database developments. JPV contributed essential tools for data analysis. RVM, JAP and CT designed and performed C. elegans experiments. CN conceived and supervised experiments. FXL and CN wrote the manuscript. All authors read and approved the final manuscript. Competing interests The authors declare that they have no competing interests. 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