Fyn kinase genetic ablation causes structural abnormalities in mature retina and defective Müller cell function

•Fyn is a pleiotropic Src-tyrosine kinase highly expressed in brain neurons and glia.•We evaluate the functional role of Fyn in the retina.•Fyn is expressed in Müller cells in vivo and in Müller-enriched primary cultures.•Fyn deficiency alters retinal morphology and adhesion properties of Müller cells.•Fyn deficiency parallels a decreased optokinetic response to visual stimuli in vivo.

Fyn kinase is widely expressed in neuronal and glial cells of the brain, where it exerts multiple functional roles that affect fundamental physiological processes. The aim of our study was to investigate the, so far unknown, functional role of Fyn in the retina. We report that Fyn is expressed, in vivo, in a subpopulation of Müller glia. We used a mouse model of Fyn genetic ablation and Müller-enriched primary cultures to demonstrate that Fyn deficiency induces morphological alterations in the mature retina, a reduction in the thickness of the outer and inner nuclear layers and alterations in postnatal Müller cell physiology. These include shortening of Müller cell processes, a decrease in cell proliferation, inactivation of the Akt signal transduction pathway, a reduced number of focal adhesions points and decreased adhesion of these cells to the ECM. As abnormalities in Müller cell physiology have been previously associated to a compromised retinal function we evaluated behavioral responses to visual stimulation. Our results associate Fyn deficiency with impaired visual optokinetic responses under scotopic and photopic light conditions. Our study reveals novel roles for Fyn kinase in retinal morphology and Müller cell physiology and suggests that Fyn is required for optimal visual processing.