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The cone photoreceptor cyclic nucleotide-gated (CNG) channel is essential for central and color vision and visual acuity. Mutations in the channel subunits CNGA3 and CNGB3 are associated with achromatopsia and cone dystrophy. We investigated the gene expression profiles in mouse retina with CNG channel deficiency using whole genome expression microarrays. As cones comprise only 2 to 3% of the total photoreceptor population in the wild-type mouse retina, the mouse lines with CNG channel deficiency on a cone-dominant background, i.e.  Cnga3 −/− /Nrl −/−   and  Cngb3 −/− /Nrl −/−   mice, were used in our study. Comparative data analysis revealed a total of 105 genes altered in  Cnga3  −/−  /Nrl −/−   and 92 in  Cngb3 −/− /Nrl −/−   retinas, relative to  Nrl −/−   retinas, with 27 genes changed in both genotypes. The differentially expressed genes primarily encode proteins associated with cell signaling, cellular function maintenance and gene expression. Ingenuity pathway analysis (IPA) identified 26 and 9 canonical pathways in  Cnga3 −/− /Nrl −/−   and  Cngb3 −/− /Nrl −/−   retinas, respectively, with 6 pathways being shared. The shared pathways include phototransduction, cAMP/PKA-mediated signaling, endothelin signaling, and EIF2/endoplasmic reticulum (ER) stress, whereas the IL-1, CREB, and purine metabolism signaling were found to specifically associate with  Cnga3  deficiency. Thus, CNG channel deficiency differentially regulates genes that affect cell processes such as phototransduction, cellular survival and gene expression, and such regulations play a crucial role(s) in the retinal adaptation to impaired cone phototransduction. Though lack of  Cnga3  and  Cngb3  shares many common pathways, deficiency of  Cnga3  causes more significant alterations in gene expression. This work provides insights into how cones respond to impaired phototransduction at the gene expression levels.

human molecular genetics

Loss of cone cyclic nucleotide-gated channel leads to alterations in light response modulating system and cellular stress response pathways: a gene expression profiling study