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. 2021 Jun 11;12:657873. doi: 10.3389/fendo.2021.657873

Figure 1.

Figure 1

ADCY7 variants crystal structure. (A) The crystal structure of Gαs.VC1.IIC2 domain in complex with the substrate analog TNP-ATP based on pdb 2GVZ; ADCY5. The Asp439 residue is depicted as a red tooth stick. The adenylate cyclase inhibitor foskolin shown as green tooth sticks and the TNP-ATP substrate analog as aquamarine tooth sticks. The two manganese ions in grey. Two residues are depicted in orange are mutated in GUCY2D causing Leber congenital amaurosis 1. VC1 in salmon, IIC2 in yellow, Gαs in grey. Residues involved in VC1.IIC2 interaction shown as tooth sticks. (B) The crystal structure of the IIC2 domain based on pdb 6R4P; ADCY9. Gly1045 shown in red with a polar interaction indicated by a yellow dashed line to the backbone of residue Gly1043. Gly1043 allow a sharp turn to the loop connecting α-helix 15 and β-strand 19. Replacing Gly1045 with arginine can be predicted to prevent this turn. Residues depicted in blue are mutated in GUCY2D causing Leber congenital amaurosis 1. In the background the VC1 domain (green) can be seen. (C) Alignment of ADCY7 sequences displaying conservation from homo sapiens at the top to Drosophila melanogaster at the bottom. Asp439 indicated by an arrow. (D) Alignment of ADCY7 sequences displaying conservation from homo sapiens at the top to Drosophila melanogaster at the bottom displaying conservation of Gly1045 indicated by an arrow.