Abstract
Intu is known as a ciliogenesis and planar polarity effector (CPLANE) protein. Although roles for Intu have been reported during embryonic development and in the context of developmental disorders, its function and regulation in adult tissues remain poorly understood. Here we show that ablation of Intu specifically in kidney proximal tubules aggravates renal ischemia-reperfusion injury, and leads to defective post-injury ciliogenesis. We identify signal transducer and activator of transcription 1 (STAT1) as a novel interacting partner of Intu. In vitro, Intu and STAT1 colocalize at the centriole/basal body area, and Intu promotes proteasomal degradation of STAT1. During cell stress, Intu expression preserves cilia length and cell viability, and these actions are antagonized by STAT1 expression. Thus, we propose a role for Intu in protecting cells and tissues after injury by targeting STAT1 for degradation and maintaining primary cilia.