Note: Intro -- CONTENTS -- PREFACE -- List of Contributors -- Ciliary Trafficking in Vertebrate Photoreceptors -- Hemant Khanna* -- INTRODUCTION -- Retina -- Photoreceptors -- Vertebrate Photoreceptors: Modified Ciliary Neurons -- Phototransduction: A Ciliary Phenomenon -- Cilia in Other Cell Types Involved in Vision -- Retinal Pigment Epithelium (RPE) -- Endothelial Cells -- Anterior Segment -- CONCLUDING REMARKS -- LIST OF ABBREVIATIONS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- Zebrafish Models of Photoreceptor Ciliopathies -- Brian D. Perkins* -- INTRODUCTION -- The Photoreceptor Sensory Cilium -- Ciliopathies -- ZEBRAFISH MODELS OF CILIOPATHIES -- Intraflagellar Transport (IFT) Mutants - The Gold Standard for Ciliopathy Phenotypes -- Zebrafish Models of Bardet-Biedl Syndrome (BBS) -- Zebrafish Models of Joubert Syndrome -- The Mutant vs. Morphant Controversy -- CONCLUDING REMARKS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- Inositol Phosphatases in Retinal Ciliary Disorder -- Cathleen Wallmuth, Na Luo and Yang Sun* -- INTRODUCTION -- Phosphoinositides and Inositol Phosphatases -- OCRL -- INPP5B -- INPP5E -- CONCLUDING REMARKS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- Understanding the Pathogenesis of Neurodegeneration in Diabetic Retinopathy (DR) -- Shahna Shahulhameed1, Subhabrata Chakrabarti1, Jay K. Chhablani2 and Inderjeet Kaur1,* -- NEURODEGENERATION -- DIABETIC RETINOPATHY -- Complications of Diabetic Retinopathy -- NEURODEGENERATION IN DIABETIC RETINOPATHY -- Clinical Evidences of Neurodegeneration in Diabetic Retinopathy -- Animal Models of Neuronal Damage in Diabetic Retinopathy -- Evidence from Pathophysiology of Affected Tissue -- MECHANISMS OF NEURONAL DAMAGE IN DIABETIC RETINA -- Inflammation and Neuronal Damage -- Glial Activation, A Cellular Mechanism of Neuronal Damage. , Microglia -- Role of Oxidative Stress in Neuroinflammation and Degeneration -- Genetic Factors in Diabetic Retinopathy -- Evidence from Proteomic Analysis of Vitreous Humor in Diabetic Retinopathy -- CONCLUDING REMARKS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- Rhodopsin Traffics to the Rod Outer Segment in the Absence of Homodimeric and Heterotrimeric Kinesin-2 -- Li Jiang, Jeanne M. Frederick and Wolfgang Baehr* -- INTRODUCTION -- Ubiquitous Expression of KIF3A and KIF17 -- Early Loss of KIF3A Arrests Ciliogenesis -- Tamoxifen-Induced KIF3A Depletion in the Adult Mouse -- Rhodopsin Traffics to tamKif3a-/- rod Outer Segments -- Homodimeric Kinesin-2 (KIF17) is not Essential for Photoreceptor IFT -- CONCLUDING REMARKS -- MATERIALS AND METHODS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- The Molecular Links between Mutations in RDS and Diseases of the Retina -- Michael W. Stuck, Shannon M. Conley and Muna I. Naash* -- INTRODUCTION -- RDS PROTEIN, TERTIARY STRUCTURE AND COMPLEX FORMATION -- RDS AND RETINITIS PIGMENTOSA -- RDS AND MACULAR DEGENERATION -- CONCLUDING REMARKS -- ABBREVIATIONS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- Rhodopsin-Regulated Grb14 Trafficking to Rod Outer Segments: Functional Role of Grb14 in Photoreceptors -- Raju V.S. Rajala* -- INTRODUCTION -- Grb14 Role in Insulin Receptor Signaling -- Negative Regulatory Role of Grb14 on Insulin Receptor Signaling -- Light-Dependent Translocation of Grb14 in Rod Photoreceptor Cells -- Cross-Talk between Rhodopsin Activation and Grb14 Signaling -- CONCLUDING REMARKS -- LIST OF ABBREVIATIONS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- Cellular Mechanisms of Cone Defects in Cyclic Nucleotide-Gated Channel Deficiency -- Xi-Qin Ding1,*, Hongwei Ma1, Martin Biel2 and Stylianos Michalakis2 -- INTRODUCTION. , Mutations in Cone CNG Channel Subunits and Human Cone Diseases -- Cone Defects in Mouse Models of CNG Channel Deficiency -- Mechanisms of Cone Degeneration Due to CNG Channel Deficiency -- Endoplasmic Reticulum Stress-Associated Cone Death -- cGMP Accumulation and Cone Death in CNG Channel Deficiency -- Mitochondrial Insult in CNG Channel Deficiency -- CONCLUDING REMARKS -- CONFLICT OF INTEREST -- ACKNOWLEDGEMENTS -- REFERENCES -- SUBJECT INDEX.