A major interest of the Miner laboratory is the role of basement membrane components in kidney function and disease, with particular emphasis on the glomerular basement membrane (GBM) as a component of the glomerular filtration barrier to albumin. Several genetic and acquired diseases of the kidney affect the GBM, causing thinning or thickening. They are focusing on the laminin and type IV collagen components of the GBM that are mutated in Pierson syndrome (a congenital nephrotic syndrome) and Alport syndrome (hereditary glomerulonephritis), respectively. They have produced knockout mice lacking relevant laminin or collagen IV chains to determine their functions in the kidney and elsewhere. They have also generated transgenic mice expressing mutant versions of laminin beta2 to understand why the mutations cause human kidney disease, using both standard transgenesis and CRISPR/Cas9-mediated appraoches. They have performed proof-of-principle studies to show that the abnormal GBM that is present in Alport syndrome can be normalized by restoring expression of the missing collagen IV network.