Page 178 - ebook

[B. Cell Biology/Stem Cell] B-24

Deficiency of TAZ reduced ciliogenesis in renal glomeruli.

Jae Hee Jun¹, Minah Park¹, Gyuyeong Rha¹, Yejin Ahn¹, Jin-Ui Min¹, Jong Hoon Park¹*

¹Department of Biological Science, Sookmyung Women`s University, Yongsan-gu, Seoul 04310, Korea

The primary cilia are antenna-like organelles and transmit the extracellular signals to cell that maintain cellular
homeostasis with the Shh, Wnt, Notch, and mTOR signaling pathways. In the case of ciliary defect, there are various

diseases polydactyly, sensorineural deafness, renal fibrosis and inflammation, cystic renal disease, and retinal
degeneration without cilia in sensory organs such as kidney, brain, and pancreas, etc. Thus, research for following

to regulate primary cilia is important. The most representative ciliary defect case in kidney is polycystic kidney
disease. This disease forms cysts full of fluid and loses renal function along with various complications, which

requires continuous dialysis or kidney transplantation. Recent studies have revealed that the hippo signaling is
associated with primary cilia and cystic diseases, and YAP, hippo signaling key regulator, involved in ciliogenesis by

modulating actin remodeling factors. In this study, we investigated the mechanism by TAZ deficiency which is
orthologous YAP, affects primary cilia formation in each renal tubule type. Little is known about the function of TAZ

regulating ciliogenesis and independent from YAP. We discovered TAZ defect reduced primary cilia only in
glomerular cells not renal collecting duct cells or proximal tubule cells. Although our study focused on TAZ,

ciliogenesis, and