Structural complementarity facilitates E7820-mediated degradation of RBM39 by DCAF15

January 1, 2020

Titrations of BodipyFL-E7820 (4) were carried out by mixing 200 nM biotinylated Strep-II-Avi-tagged DCAF15 variants or an equivalent volume of the assay buffer, 2 nM terbium-coupled streptavidin in the same assay buffer. After dispensing the assay mixture, an increasing concentration of BodipyFL-E7820 (4) was dispensed in the 384-well plate using a Titrations of BodipyFL-E7820 (4) were carried out by mixing 200 nM biotinylated Strep-II-Avi-tagged DCAF15 variants or an equivalent volume of the assay buffer, 2 nM terbium-coupled streptavidin in the same assay buffer. After dispensing the assay mixture, an increasing concentration of BodipyFL-E7820 (4) was dispensed in the 384-well plate using a Titrations of BodipyFL-E7820 (4) were carried out by mixing 200 nM biotinylated Strep-II-Avi-tagged DCAF15 variants or an equivalent volume of the assay buffer, 2 nM terbium-coupled streptavidin in the same assay buffer. After dispensing the assay mixture, an increasing concentration of BodipyFL-E7820 (4) was dispensed in the 384-well plate using a D300e digital dispenser normalized to 2% DMSO and then incubated for 15 min at room temperature. normalized to 2% DMSO and then incubated for 15 min at room temperature. normalized to 2% DMSO and then incubated for 15 min at room temperature

The investigational drugs E7820, indisulam and tasisulam (aryl-sulfonamides) promote the degradation of the splicing factor RBM39 in a proteasome-dependent mechanism. While the activity critically depends on the cullin RING ligase substrate receptor DCAF15, the molecular details remain elusive. Here we present the cryo-EM structure of the DDB1-DCAF15-DDA1 core ligase complex bound to RBM39 and E7820 at a resolution of 4.4 Å, together with crystal structures of engineered subcomplexes. We show that DCAF15 adopts a new fold stabilized by DDA1, and that extensive protein-protein contacts between the ligase and substrate mitigate low affinity interactions between aryl-sulfonamides and DCAF15. Our data demonstrate how aryl-sulfonamides neo-functionalize a shallow, non-conserved pocket on DCAF15 to selectively bind and degrade RBM39 and the closely related splicing factor RBM23 without the requirement for a high-affinity ligand, which has broad implications for the de novo discovery of molecular glue degraders.

Faust, TB; Yoon, H; Nowak, RP; Donovan, KA; Li, Z; Cai, Q; Eleuteri, NA; Zhang, T; Gray, NS; Fischer, ES;

Journal: Nat. Chem. Biol. Pages: 7-14

Original article (31686031)