NEUROSCIENCE. For the article “AIPL1, the protein that is defective in Leber congenital amaurosis, is essential for the biosynthesis of retinal rod cGMP phosphodiesterase,” by Xiaoqing Liu, Oleg V. Bulgakov, Xiao-Hong Wen, Michael L. Woodruff, Basil Pawlyk, Jun Yang, Gordon L. Fain, Michael A. Sandberg, Clint L. Makino, and Tiansen Li, which appeared in issue 38, September 21, 2004, of Proc. Natl. Acad. Sci. USA (101, 13903–13908; first published September 13, 2004; 10.1073/pnas.0405160101), the authors note that “r/r_peak” incorrectly appeared as “pA” for the ordinate label in Fig. 5B. The corrected figure and legend appear below. This correction does not affect the conclusions of the article.

Fig. 5.

Photoresponses of single rods. (A) Averaged, normalized flash responses of a mutant rod (thick traces) and a WT rod (thin traces). The maximum response amplitude was 11.4 pA for the mutant rod and 15.9 pA for the WT rod. (B) Averaged single-photon responses of mutant (thick trace) and WT (thin trace) rods. Averaged dim flash responses from mutant and WT rods were scaled to the average ratio of the ensemble variance to mean amplitude for rods of each type and then normalized by 0.65 pA, the mean value obtained for the mutant rods. Flashes generating responses with mean amplitudes <0.2 r_max were considered to be dim. The times to peak were 215 and 130 msec, and the integration times were 545 and 259 msec for the mutant and WT rods, respectively. (C) Stimulus-response relations of cells in A. Results were fit with: r/r_max = 1 - exp(-ki), where i is the flash strength, k is ln(2)/i_1/2, and i_1/2 is the flash strength producing a half-maximal response. i_1/2 values were 28 and 50 photons μm^-2 for the mutant and WT rods, respectively.