 Hello, my name is Raul Esteved. I am a professor of physiology in the Faculty of Medicine at the University of Barcelona. Our group is working in the molecular basis of a type of leukodystrophy called megalencephalic leukonsophalopathy which is a cortical disease. This disease is diagnosed on the basis of a specific clinical phenotype and also on a specific MRI abnormalities. So basically there are defined two groups of patients. Most show anaerological deterioration and the rest lack clinical deterioration and show a major improvement on magnetic resonance imaging. Our group in collaboration with the group of Marge van der Knap from Amsterdam have identified and characterized most of the mutations identified in the two genes related with the disease which are called mlc1 and gliarcane. The function of these two proteins is still unknown, although our work has related the function of these proteins with the regulation of glial chloride fluxes in the brain. And it seems that the regulation of these processes is important for some physiological functions such as the control of volume regulation and the process of potassium symphony. Hello my name is Neyta Neda and I am the first author of this paper. In this work we have analyzed biochemically and functionally most mutations identified up to date in apacam. We have classified the effect of these mutations in different subtypes. Some mutations affect glial-cane protein expression and its arrival to the plasma membrane. Most mutations reduce the localization in cells and junctions. In this work we have found two different mechanisms that leads to this effect in targeting. Some mutants affect its ability to homolygomerize and the other ones may affect transomophilic interactions. We have also identified a mutation that is mislocalized in astrocytes from the mlc knockout mouse, suggesting that both proteins rely on each other to be stable. Finally we have found some mutations that act as a gain-of-function mutants showing an effective internalization in mlc knockout astrocytes treated with hypotation conditions. Thank you for listening. So we believe that the study of these mutants will be very important to solve two main questions that remained on mlc research. Why some apacam mutations behave as dominant and others as recessive? And more importantly, what is the molecular role of mlc-1 on anglial-cane? We hope that these questions will be solved in the near future. So please don't hesitate to contact me if you need further explanations about this work. Bye-bye!