The Journal of Neuroscience, June 21, 2006, ():
Phototransduction in a Transgenic Mouse Model of Nougaret Night Blindness
J. Neurosci. Moussaif et al.
26: 6863
Supplemental data
Files in this Data Supplement:
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Supplemental Fig. 1. Diagram of potential conformational perturbations disrupting the GTPase activity and RGS9/effector binding sites in the G38D mutant. Tα residues 35-41 (phosphate-binding loop, P-loop), 199-211 (switch II), 238-249 (α3 helix) (yellow tube), RGS9-1 residues 359-366 (magenta tube) and Pγ residues 63-74 (pink tube) are shown from the TαGDPAlF4-•Pγ•RGS9 complex structure (Slep et al., 2001). The conformational changes induced by the G38D mutation are modeled on the basis of the Gia1G42V structure (Raw et al., 1997) using SWISS-model (Guex and Peitsch, 1997). (A) The key catalytic residue Q200 (green sticks) interacts with the crucial RGS9 GAP residue, N364. The substitution of G38 by D (cyan sticks) forces Q200 (red sticks) out of the active site for GTP hydrolysis and into position where it may clash with N364. (B). The G38D substitution causes the side chain of R201 (green sticks) to rotate (red sticks), thereby disrupting its contacts with Pγ V66 and I67, and weakening the switch II/α3 linkage in Tα. The images were generated using PyMOL (v 0.97) (DeLano, 2004).
