To understand the pathways and interactions between different cell types in the glomerulus that are critical to set up the filtration barrier Dr. Quaggin’s research team has developed a number of genetic tools that permit cell and time-specific manipulation of gene expression. Using these tools, her lab has shown that VEGF-A is a major angiogenic factor required in the glomerulus. 'Tweaking' the dose of VEGF-A within the glomerulus leads to distinct and dramatic glomerular phenotypes during development and in adult mice. These phenotypes resemble a variety of glomerular lesions from preeclampsia, to focal segmental glomerulosclerosis, two major causes of renal disease in patients. Loss of all VEGF-A within the glomerulus results in a complete failure of the filtration barrier to form. Dr. Quaggin's lab is currently dissecting the upstream and downstream effectors of the VEGF-A signaling pathway that include the transcription factor, Pod1, and the Von Hippel Lindau tumour suppressor gene.