Disrupted glucocorticoid receptor cell signalling causes a ciliogenesis defect  in the fetal mouse renal tubule
Primary cilia are microtubule-based organelles essential for cell signaling and environmental sensing, playing vital roles in embryogenesis and tissue homeostasis. In the kidney, they function as fluid sensors on tubular epithelial cells, and defects in their structure or function lead to ciliopathies like polycystic kidney disease (PKD). This study demonstrates that glucocorticoid receptor (GR) signaling is crucial for normal cilia formation in mouse and human renal tubules. RNA sequencing of GR-null mouse kidneys revealed significant downregulation of ciliogenesis-related genes (Ccp110, Cep97, Cep290, Kif3a), while confocal microscopy showed stunted cilia in proximal tubules, podocytes, and collecting ducts. Activation of GR with dexamethasone increased cilia length in human kidney organoids and mouse renal cells, an effect reversed by the GR antagonist RU486. GR-null kidney extracts exhibited reduced pERK and SUFU levels, indicating pathway crosstalk in ciliogenesis regulation. Additionally, dexamethasone lowered Aurora kinase A, a cilia disassembly factor implicated in PKD.