in pathway in some patients. However, we ” still think it is an important mechanism. Because RP is a late onset and slowly progressive disease, patients usually have no obvious symptoms in 
childhood with no complains. In our research, the average age when patients were diagnosed with RP is 35 years old, and visual loss progresses very slowly leading to blindness. So prevention of any pathway of rod photoreceptor cell death would be a great help in maintaining a patient’s quality of life. However, to date, there are no effective cell protection therapies. The cell death pathway that we have demonstrated includes novel target molecules, adenylyl cyclase and PKA, and may be helpful in developing an effective drug treatment for RP. Statement for the Use of Animals in Ophthalmic and 1702259-66-2 Vision Research. All animal “9226994 experiments were carried out under approved protocols and in accordance with the recommendations for the proper care and use of laboratory animals by the Committee for Animals, and Infectious Pathogens Experiments at Kyushu University and according to The Law and Notification of the Japanese Government. In the sections below, n is used to indicate the number of treated eyes. Molecular biology PCR was carried out in a 50 ml reaction mixture containing 100 ng of genomic DNA, 50 pmol of each primer, 2.0 mM MgCl2, 16 reaction buffer, 200 mM of each dNTP, and 1.0 U of Ex TaqH polymerase. Samples were amplified for 30 cycles, 30 s at 94uC, 30 s at 60uC, and 30 s at 72uC. Total RNA was extracted from embryos using ISOGEN and prepared for cDNA synthesis using SuperScriptHII transcriptase. Reverse transcription was performed in a 20 ml reaction volume, containing,1 mg total RNA, 500 ng Oligo1218, 500 mM of each dNTP, 10 mM DTT, and 50 units of SuperScriptHII at 42uC for 50 min. PCR conditions were essentially the same as in the genomic PCR described above except the annealing temperature was changed from 58uC to 62uC, and the extension time was changed from 30 s to 5 min. PCR was performed with gene-specific primers. PCR products were purified using the QIAquickH PCR Purification Kit following the user manual and sequenced. Mutations were detected by direct sequencing. The primers used are as follows: b-Actin, 59-TGGTATTGTGATGGACTCTGG-39 and 59-AGCACTGTGTTGGCATACAGG-39; Transducin a, 59-ATCAAAAGTCAGTATGGGGGCCGG-39 and 59-CTGTGCGGCAGCGTCTCCATAG-39; PDE6b, 59-CTCCAGACTCTGAGATCGTC-39 and 59-CACAGTTGTGAAGGTAGCTC-39; ADCY2B, 59-CGCCTTGATCCTCTGCATTTGTTT-39 and 59CCCGGCCGGTCTGGTTG-39; ADCY2B, 59-TGGCGAGGCAGAATGAATA-39 and 59-TACTGCCGGTCGTGATACTG-39; Transgenic ADCY2B tail, 59-ATAAAGAGGGGTTGGAGTGT-39 and 59-TGTGGTATGGCTGATTATGATC39; Transgenic rhodopsin Q344X, 59-CCAGCGTGGCATTCTACATC-39 and 59-AACGCTTACAATTTACGCCT-39. Morpholino Knock Down Morpholino oligonucleotide knock downs were performed as described previously. The concentration of MOs used in the experiments is 380 mM. For each gene, we used a morpholino targeted to a splice site of the genes. These morpholinos block the splicing and the efficiency of SP morpholino knock down was determined by RT-PCR analysis. The following morpholinos were used: Transducin a, 59-CAGCACCTGAAAGCAAGACAGTGTT-39; Transducin a, 59-TCTGGGATGGAGAAAGATACGTTTA-39; PDE6b, 59-GACTGTCCTACAGCGAAAACAAAGT-39; and Standard Control Morpholino, 59CCTCTTACCTCAGTTACAATTTATA-39. Materials and Methods Fish Strains The maintenance and breeding of zebrafish strains and staging of embryonic development were performed as described. The ovl
