Frizzled (FZD) receptors tightly regulate different biological processes and are involved in various diseases, including multiple cancers. Wingless/Int1 (Wnt) family proteins act as ligands for FZDs. They initiate distinct signalling pathways broadly categorized into the "canonical" or beta-catenin-dependent and the "non-canonical" pathways. At least some non-canonical pathways are mediated via FZD coupling to heterotrimeric G proteins. There is no structural information on how Wnts bind to and activate full-length FZDs. However, due to high levels of constitutive activity, there are now multiple structures of FZD receptors bound to G proteins in the absence of ligands.
FZD5 significantly promotes the proliferation, DNA damage repair, and stemness of chemo-resistant triple-negative breast cancer. Additionally, FZD5 drives epithelial-mesenchymal transitions and tumorigenesis in various cancer types, highlighting its potential as a valuable therapeutic target. To understand the structural basis for FZD5 activation and G protein coupling, we determined the first cryo-electron microscopy structure of the FZD5-mGq complex to 2.7 Å resolution. The FZD5-mGq structure closely resembles those of other FZD-G protein complexes. The N-terminal CRD domain was visualized at a lower (6 Å) resolution for the first time. However, the G protein adopts a unique position relative to the receptor, and a unique density was observed at the receptor-G protein interaction site. Our future studies focus on understanding the FZD-G protein coupling and the role of CRD in FZD receptor activation.