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Irreversible photoreceptor cell death is a major cause of blindness in many retinal dystrophies. A better understanding of the molecular mechanisms underlying the progressive loss of photoreceptor cells remains therefore crucial. Abnormal expression of microRNAs (miRNAs) has been linked with the aetiology of a number of retinal dystrophies. However, their role during the degenerative process remains poorly understood. Loss of cone photoreceptors in the human macula has the greatest impact on sight as these cells provide high acuity vision. Using a  Chrnb4-cre; Dicer   flox/flox   conditional knockout mouse (Dicer CKO) to delete  Dicer1  from cone cells, we show that cone photoreceptor cells degenerate and die in the  Dicer -deleted retina. Embryonic eye morphogenesis appeared normal in Dicer CKO mice. Cone photoreceptor abnormalities were apparent by 3 weeks of age, displaying either very short or absent outer segments. By 4 months 50% of cones were lost and cone function was impaired as assessed by electroretinography (ERG). RNAseq analysis of the Dicer CKO retina revealed altered expression of genes involved in the visual perception pathway. These data show that loss of  Dicer1  leads to early-onset cone cell degeneration and suggest that  Dicer1  is essential for cone photoreceptor survival and homeostasis.

Conditional Dicer1 depletion using Chrnb4-Cre leads to cone cell death and impaired photopic vision