Context
Kidneys are two bean-shaped organs located on either side of the body. They play essential roles in maintaining homeostasis by filtering the blood, removing waste products, and producing urine. Blood enters the kidneys through the renal arteries and leaves through the renal veins. Each kidney connects to a ureter, which transports urine to the bladder.
Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disorder most often caused by mutations in the genes encoding polycystin-1 (PC1) or polycystin-2 (PC2). It is characterized by the formation of numerous fluid-filled cysts in the kidneys, leading to complications such as hypertension, kidney stones, recurrent urinary tract infections, and ultimately kidney failure. ADPKD affects approximately 12 million people worldwide. There is currently no cure, and cyst formation cannot be halted.
It has recently been shown that Glis transcrition factor family plays important roles in ADPKD1. Specifically, we observed Glis3 as a modifier of ADPKD as the dual inactivation of Glis3 and Pkd1 significantly worsened polycystic kidney phenotype. This was carried out using a specific method using Precellys Evolution that allow nuclei isolation from wildtype and pre-cystic kidneys for ATAC-seq in a midi-throughput fashion.
This application note will describe the method of generating nuclei amenable for ATAC-seq in a midi-throughput way from mouse kidney tissue.
