Structure-function analysis of β-arrestin Kurtz reveals a critical role of receptor interactions in downregulation of GPCR signaling in vivo.

ABSTRACT: Arrestins control signaling via the G protein coupled receptors (GPCRs), serving as both signal terminators and transducers. Previous studies identified several structural elements in arrestins that contribute to their functions as GPCR regulators. However, the importance of these elements in vivo is unclear, and the developmental roles of arrestins are not well understood. We carried out an in vivo structure-function analysis of Kurtz (Krz), the single ortholog of mammalian β-arrestins in the Drosophila genome. A combination of Krz mutations affecting the GPCR-phosphosensing and receptor core-binding ("finger loop") functions (Krz-KKVL/A) resulted in a complete loss of Krz activity during development. Endosome recruitment and bioluminescence resonance energy transfer (BRET) assays reveale

SUBMITTER: Chai F 

PROVIDER: S-EPMC6842422 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature