Glomerular Diseases of the kidney are the major causeof FSGS (Focal segmentalglomerulosclerosis) and ESRD (end stage renal disease) in the UnitedStates. Glomerular podocytes that contribute to the kidney filter have afoot-like appearance with numerous interdigitating processes that arise fromtheir cell bodies and completely cover the glomerular basement membrane.Various studies have suggested that podocytes are a major target in glomerulardiseases including nephrotic syndromes, diabetic nephropathy, FSGS (focalsegmental glomerulosclerosis) and their dysfunction is associated withproteinuria and loss of kidney function. Our earlier investigated suggested the dynamic nature of Neph1, whichunder pathophysiological conditions removed from the cell-cell junctionand at recovery localized at the cell membrane as normal condition. This study is aimed at investigating thehypothesis that the dynamic interactions between novel slit-diaphragm proteinsMyo1c and Neph1 are critical for the maintenance of slit diaphragm integrity byusing in-vivo and in-vitro model system. My focuswill be on elucidating the intracellular signaling pathways that are inducedfollowing podocyte injury that regulate changes in podocyte morphology orjunction formation with the long term goal of identifying therapeutic targets.As a part of this project I am using Mice and Zebrafish as a model of kidneydisease. This will provide important information to understand the molecularmechanisms leading to the development of glomerular diseases that will revealnew therapeutic approaches.