The aim of my master project has been to look for genetic interactions between mutations of the genes encoding the Elba complex and the Fab-7 boundary that is crippled by the mutations in the 5 GAGAG sites of HS1. Knowing that phenotypes caused by mutations can be hidden by maternal contribution and that the mutant we recovered are not homozygous viable, I have also generated mutant flies in which the genes are inactivated by RNAi. Using this method combined with a Fab-7 boundary mutant for its GAGAG binding sites within HS1, I observed an aggravation of the Fab-7 phenotype with high penetrance with every gene inactivation.