Gene expression differences between wildtype and Atrx conditional knockout mouse retina tissues. Mus musculus

Loss of the Atrx chromatin remodeling protein causes dysfunction and death of post-mitotic retinal interneurons in mice. Embryonic conditional deletion of Atrx from multipotent retinal progenitor cells results in the selective loss of the retinal inhibitory interneurons, namely amacrine and horizontal cells. The cell death occurs postnatally after the development of these cell types, peaking at postntal day 17 in the mouse retina. Identification of molecular factors and pathways that mediate the health and survival of these neurons may suggest novel therapeutic strategies for neuroprotection in ATR-X syndrome and other neurodegenerative diseases. We performed gene expression profiling of wildtype and Atrx conditional knockout mouse retina tissues to identify putative targets of Atrx and molecular pathways that underlie the neurodegenerative phenotype. Overall design: Mouse retinas were isolated from Chx10Cre-mediated Atrx cKO and wildtype (Cre-) littermates at postnatal day 17 (P17) for RNA extraction and hybridization to Affymetrix mouse gene microarrays. P17 is the age at which the peak of retinal amacrine and horizontal cell neurodegeneration is reached in the Atrx cKO mice.