title: Fyn kinase genetic ablation causes structural abnormalities in mature retina and defective Müller cell function.
abstract: 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.
authors.affiliation: Departamento de Farmacobiología, CINVESTAV-Sede Sur, México D.F, México.
authors.forename: Marbella
authors.initials: M
authors.lastname: Chavez-Solano
authors.affiliation: Departamento de Farmacobiología, CINVESTAV-Sede Sur, México D.F, México.
authors.forename: Alfredo
authors.initials: A
authors.lastname: Ibarra-Sanchez
authors.affiliation: Laboratorio de Plasticidad Cortical y Aprendizaje Perceptual, Instituto de Neurociencias, Universidad de Guadalajara, México.
authors.forename: Mario
authors.initials: M
authors.lastname: Treviño
authors.affiliation: Departamento de Farmacobiología, CINVESTAV-Sede Sur, México D.F, México.
authors.forename: Claudia
authors.initials: C
authors.lastname: Gonzalez-Espinosa
authors.affiliation: Departamento de Farmacobiología, CINVESTAV-Sede Sur, México D.F, México. Electronic address: mlamas@cinvestav.mx.
authors.forename: Monica
authors.initials: M
authors.lastname: Lamas
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D049109:Cell Proliferation; D002478:Cells, Cultured; D063928:Ependymoglial Cells / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051076:Proto-Oncogene Proteins c-fyn / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction; D014785:Vision, Ocular
chemical_list: C494960:Fyn protein, mouse; D051076:Proto-Oncogene Proteins c-fyn; D051057:Proto-Oncogene Proteins c-akt
keywords: Akt kinase; FAK; Fyn kinase; Müller glia; Optokinetic response; Retina