FZD receptors tightly regulate different biological processes and are involved in different cancers [1]. Wingless/Int1 (WNT) family proteins act as ligands for FZDs. They initiate distinct signalling pathways broadly separated into the "canonical" or beta-catenin-dependent and the "non-canonical" pathways [2], [3]. At least some of the non-canonical pathways are mediated via FZD coupling to heterotrimeric G proteins. As all class F G protein-coupled receptors, FZD have a long extracellular N-terminal cysteine-rich domain (CRD) and a seven-transmembrane domain (7TM). While individual structures of CRD-Wnt complexes and individual 7TM have been determined, there is no structural information on how WNTs bind to and activate full-length FZDs or what conformation CRD adopts upon receptor activation. SAG1.3 is a Smoothened receptor agonist that also activates FZD receptors[4]. Due to challenges with WNTs' hydrophobic nature and stability, we decided to use SAG1.3 to examine the molecular details of FZD activation.
We co-expressed FZD7-mGs complex in insect cells and purified it in the presence of SAG1.3. The purity and composition of the complex were confirmed by the Coomassie-stained gel and the Western blot. Complex formation was further confirmed by negative-stain electron microscopy. The high-resolution dataset was collected using a Titan Krios microscope and yielded a 2.6Å map. Unfortunately, no SAG1.3 or CRD were observed, most likely due to the low affinity of SAG1.3 and the flexibility of the FZD CRD domain. Currently, we are investigating whether other G proteins might form more stable complexes with FZD7 and SAG1.3 (by looking at FZD7-mGi complexes) or whether CRD flexibility might be reduced in other FZD receptors (FZD5-mGq complexes).